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Word pain is derived from a Greek word “Poine” which mean penalty or punishment Pain is a protective mechanism that occurs when tissues are being damaged. It causes the individual to remove the painful stimulus. It is probably the most fundamental and primitive sensation, distributed more or less all over the body. DEFINITION OF PAIN According to International Association for the Study of Pain (IASP) pain is defined as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”.





Each of these components can occur in isolation or in varying combination and proportions.

Each of these components can occur in isolation or in varying combination and proportions. The sensory component describes how the pain feels (i.e.,) it may be sharp, aching or related to the cause. Eg., Burning, stabbing etc., The affective or emotional component of pain refers to the emotional distress caused by the pain (i.e.,) it hurts. The autonomic component relates to the changes, which occur in the body. Eg., alteration in heart rate, blood pressure or body temperature. The motor component refers to the withdrawal of the injured limb from the stimulus. This is known as reflex and is accompanied by vocalization and facial grimacing. FUNCTIONS OF PAIN The function of pain is to alert the body to tissue injury before serious damage can occur and in this context it has both protective and survival value.

Pain experience enables prevention of further damage by withdrawal and avoidance of pain stimulus. Pain also promotes healing and recovery following injury as it limits activity, ensuring that the affected area is rested. This promotes repair of the tissues and prevents further exacerbation of the injury. PAIN CAN BE FELT AS     

Superficial or deep pain Referred pain Projected pain Intractable pain Psychogenic pain

SUPERFICIAL OR DEEP PAIN Superficial pain occurs when the receptors in the surface tissues are stimulated, and it has a sharp distinct quality.

Deep pain is divided into SPLANCHNIC PAIN – occurring deep in the viscera SOMATIC PAIN -which occurs in structures such as muscles, tendons, joints and periosteum. A feature of visceral pain is that it is referred to other parts of the body(for instance cardiac pain is felt in the arm). REFERRED PAIN Pain arising from deep tissues, the muscles, ligaments, joints and viscera is often perceived at a site distant from the actual nociceptive source. Thus, the pain of angina pectoris is often perceived in the shoulder or neck.

Pain from musculoskeletal and visceral sources is usually deep, dull, aching and more diffuse. MECHANISM SYMPATHETIC TERMINALS appear to release at least two types of prostaglandins in response to bradykinin and in areas of injury or inflammation, in response to nor-epinephrine. With respect to referred pain, it is postulated that efferent sympathetic impulses release similar substances that sensitize the afferent noci-ceptors in the areas of referred pain. Alternatively, sympathetic nerve activity in the area of referred pain may cause vasoconstriction that comprises the nourishment to the afferent nociceptor itself. Ischaemia lowers the firing threshold of nerves. ANATOMIC STUDIES have demonstrated that some distal root ganglion cells have peripheral branches supplying two remotely different sites. The brain may misinterpret the nociceptive input from the branch as coming from the other. CONVERGENCE PROJECTION THEORY This is the most popular theory. Primary afferent nociceptors 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 of visceral structures through past experience interprets the pain as coming from the regions subserved by the cutaneous afferent fibers CONVERGENCE–FACILITATION THEORY This theory is similar to the convergence projection theory except that the nociceptive input from the deeper structures causes the resting activity of the

second–order pain transmission neuron in the spinal cord to increase or be ‘facilitated’. The resting activity is normally created by impulses from the cutaneous afferents. ‘Facilitation’ from the deeper noci-ceptive impulses causes the pain to be perceived in the area that creates the normal resting background activity. PROJECTED PAIN This occurs when pain messages are set up at a point along the pain pathway beyond the peripheral pain receptors.

Intractable Pain This refers to any persistent severe pain that cannot effectively be controlled by normal medication.

Psychogenic pain This refers to the pain for which there is no detectable organic lesion or peripheral stimulation. The discomfort is very real to the individual and is thought to be the physical manifestation of a psychological disturbance. TYPES OF PAIN    

Pain on a broad scale is divided into Fast pain or acute pain Slow pain or chronic pain Transient pain

ACUTE PAIN Acute pain is characterized by a well defined time of on-set and is associated with both subjective and objective signs indicating activation of sympathetic

nervous system. Usually resolves once the cause is removed and healing has occurred. CHRONIC PAIN Chronic pain persist long after healing has occurred and is associated with both physiological and behavioral changes. At these stages the pain is not serving any useful function and may result in levels of activity and function being governed by the pain. TRANSIENT PAIN Transient pain has a short duration. In transient pain there are two types of pain experienced. The first is mild and localized and is followed by a more diffuse intense pain, which may decrease in intensity. These pains are commonly associated with minor injuries.

FAST PAIN It is a short, well localized, stabbing sensation which is acute and is matched to the stimulus, such as pin prick,surgical skin incision. This pain starts abruptly when stimulus is applied Ends promptly when stimulus is removed. It results from stimulation of small myelinated A-δ fibres having a diameter of 2-5 ¾m, conduction velocity at the rate of 12-30 m/sec. Because of this high conduction velocity these fibres are called FAST FIBRES. Not felt in most of the deeper tissues of the body. SLOW PAIN

It is throbbing, burning,aching sensation which is chronic and poorly localized. This is less specifically related to stimulus. pain may continue long after removal of stimulus. Results from stimulation of more primitive, unmyelinated type - C nerve fibers with conduction velocity 0.5 – 2m/sec and diameter 0.4-1.2 µm. Due to this slow conduction velocity,C fibres are called as SLOW FIBRES. This type of pain is usually associated with tissue destruction. It can occur both in the skin and in almost any internal tissue or organ.

PAIN RECEPTORS Pain can arise from stimulation of pain receptors / nociceptors. Pain receptors are free, afferent nerve endings of myelinated A-δ and unmyelinated C-fibres that encode the occurrence, intensity duration and location of noxious stimuli and signal pain sensation. In contrast to other sensory receptors pain receptors do not adapt. This is a protective mechanism because it allows the individual to remain aware of continual tissue damage. THREE CATEGORIES OF PAIN RECEPTORS MECHANO SENSITIVE PAIN RECEPTORS: excited by excessive mechanical stress or mechanical damage. THERMOSENSITIVE PAIN RECEPTORS: sensitive to extreme heat or cold.

CHEMOSENSITIVE PAIN RECEPTORS: sensitive to various chemical substances Eg., bradykinin, serotonin, histamine, potassium ions, acids, prostaglandins, acetylcholine & proteolytic enzymes. HYPERALGESIA Hyperalgesia is a decrease in pain threshold in an area of inflammation, such that even trivial stimuli cause pain. It is most likely due to local release of chemical mediators from injured cells in the inflammed area, resulting in the sensitization of pain receptors. The metabolites of arachidonic acid and bradykinin appear to play an important role in sensitization of pain receptors.

(Trauma to tissue leads to local response of multiple chemical substances (substance P (sp), Prostaglandins PgE, bradykinin, BK, serotonin 5HT from a cascade of archidonic acid metasolites from afferent nerve endings resulting in vasodilatation, increase vascular permeability and sensitization of nociceptors)

Hyperalgesia may well develop from release of Dynorphin a newly discovered opioid peptide found at the site of injury. Dynorphin also widens the neurons receptive field beyond the immediate injury site. Allodynia – Pain from stimuli that are normally not painful. THEORIES OF MECHANISM OF PAIN TRANSMISSION Three of many theories explaining mechanism of pain transmission are • Specificity theory • Pattern theory • Gate control theory THE SPECIFICITY THEORY (VON FREY,1894) It states that different sensory fibres mediate different sensory modalities such as pain, heat, cold, touch and pressure. The receptor for pain are specific and are mostly unmyelinated free nerve endings. When stimulated these fibres transmit impulses along specific pathways. THE PATTERN THEORY Pain is generated by non-specific receptors. It assumes that all nerve fibre endings are alike and that the pattern for pain is produced by a more intense stimulation than for other sensations. The summation of the pain impulses produce a pattern that the brain receives and recognizes. GATE CONTROL THEORY (Melzack and Wall) According to this theory two factors that regulate pain transmission are:

A gating mechanism located in a specific area of gray matter in the spinal cord is called the substantia gelatinosa. This gating mechanism receives painful impulses from peripheral nerves and permits their passage to the brain by opening the gate, or prevents their passage by closing the gate. Whether the gate opens or closes depends on the speed of the impulse The interaction between noxious pain stimulus transmitted along small diameter fibres The stimuli of touch and pressure that are transmitted along the larger diameter fibres Descending central control from intrinsic brain mechanisms modulates the gating mechanism. This control arises from emotional, motivational, psychic, peripheral and visual stimuli as well as from past learned experience. HOW THE GATE WORKS ? Axons of larger diameter afferent neurons (A-α, A-β, A-γ) enter the spinal cord through the dorsal root. The principal branch of the large diameter axon enters the dorsal horn, synapsing with T-cells. A collateral (branch) of the same fibre enters the substantia-gelatinosa and terminates on the SG cells. Another branch may ascend to the higher centres. Axons of small–diameter afferent neurons (C & A-δ) enter dorsal horn of spinal cord to synapse with T-cells. They also send a collateral to the substantia gelatinosa to terminate on the SG cells.

The SG cells send branches to synapse with incoming axon fiber entering the T-cell pool. Branches from the SG cells do not contact the T-cells directly but rather the terminal area of A & C axons. The only activity that the SG cells can do is send inhibitory impulses to the T-cells preventing them from firing an impulse.

Large diameter fibres can only excite the SG cells, which inturn send out inhibitory impulses to the T-cells. Since the T-cells are unable to transmit an impulse the GATE IS CLOSED TO PAIN. Messages from the branches of smaller A-δ and C fibres can only inhibit the SG cells, stopping them from sending inhibitory impulses to the T-cells. This action OPENS THE GATE TO PAIN. Since T-cells are not receiving inhibitory impulses from the SG cells they are free to send a painful response when activated by the smaller C or A-δ fibres. Thus smaller fibres, A- δ and C, open the gate to pain by inhibiting SG cells; larger A-α, A-β, A-γ fibre closes the gate by exciting the SG cells. Stimuli such as touch, pressure, vibration and rubbing send impulses via the large fibres which close the gate when pain is present from small fibre activity. The large diameter axons can also send an ascending collateral branch to central control, the higher centres of the brain. As a result signals from the brain,by means of descending tracts can influence the gate control. PATHWAYS FOR TRANSMISSION OF PAIN Two pathways for transmitting pain signals into the central nervous system, which corresponds to two different types of pain

 An acute – sharp pain pathway  A slow – chronic pain pathway Odontogenic pain transmission is mediated primarily by peripheral sensory neurons of the trigeminal nerve. These specialized nerve endings and their respective axons all known as PRIMARY AFFERENT NOCICEPTORS. These peripheral sensory neurons are myelinated Aδ-fibers mainly innervating dentin and ummyelinated C-fibers innervating the body of the pulp. Most of the myelinated nerve fibers of pulp are A-δ fibers. They are relatively large fibers with fast conduction velocities. They enter the root canal and divides into smaller branches coursing coronally through the pulp. PROCESSING In most cases the input from the pulpal and periradicular tissues is transmitted through the maxillary and mandibular branches of trigeminal nerve towards the CNS for processing Activation of primary afferent nociceptors is called TRANSDUCTION PROCESSING OF THE FAST PAIN SIGNALS The acute sharp pain signals are transmitted in the peripheral nerves to the spinal cord by small type of A δ fibres. They terminate at two points in the dorsal horns of the spinal cord in lamina I (lamina marginalis) lamina V

In both these laminae the incoming pain fibers excite the second order neurons that send long fibers immediately to the opposite side of the cord in the anterior commissure. And then upwards to the brain in the lateral division of the antero lateral sensory pathway. PROCESSING OF THE SLOW PAIN SIGNALS The type ‘C’ fibers that transmit the ‘slow’ pain signals terminate almost entirely in lamina II and III of the dorsal horns an area called substantia gelatinosa. Most of the signals then pass through one or more additional short fibre neuron eventually terminating,mainly in lamina V Here the last neuron in the series gives rise to long axons most of which join fibres of fast pathway Pass through anterior commissure to the opposite side of the cord upward to the brain via lateral division of antero – lateral pathway. However few of these fibres will not cross and pass ipsilaterally to the brain.

Transmission of both ‘acuteacute-sharp’ sharp’ and ‘ slowslowchronic’ chronic’. Pain signals into and through the spinal cold on the way to the brain stem.

Transmission of both ‘acute-sharp’ and ‘slow-chronic’. Pain signals into and through the spinal cold on the way to the brain stem. Termination of the fast-acute pain pathway in brainstem and thalamus About three quarters of all pain fibres terminate in reticular formation of medulla, pons and mesencephalon. From these areas higher order neurons are transmitted to the thalamus, hypothalamus and other areas of diencephelon and cerebrum However, a small proportion of the pain fibres (fast-acute type) pass directly to the thalamus From here signals are transmitted into other areas of the thalamus and also to the somato sensory cortex. These signals to cortex are important for localizing the pain, not for interpreting it. TERMINATION TERMINATION OF THE SLOW CHRONIC PAIN FIBRES IN THE BRAINSTEM AND THALAMUS These fibres terminate almost entirely in reticular formation of the brainstem. However greater number of signals are relayed upward through this formation and finally into INTRALAMINAR NUCLEI of thalamus to all areas of cerebral cortex and also laterally into basal regions of brain around the thalamus, including hypothalamus.

Transmission of pain signals into the hindbrain, thalamus and cortex via fast and slow pain pathways

Transmission of pain signals into the hindbrain, thalamus and cortex via fast and slow pain pathways Pain preception is the function of thalamus, lower centre and those involved in reticular formation. Cerebral cortex plays an important role in interpreting the quality of pain rather than pain perception. DENTAL PAIN Once beneath the odontogenic layer, the A- δ fibers lose their myelin sheath and anastomose into a network of nerves referred to as PLEXUS OF RASCHKOW This circumpulpal layer of nerves sends free nerve endings onto and through the odontoblastic cell layer extending up to 200 ¾m into the dentinal tubules

while also contacting the odontoblastic cell process. This is called PULPODENTINAL COMPLEX

C-Nerve fibers C-fibers are small un-myelinated nerves that innervate the pulp. They are high threshold fibers course centrally in the pulp stroma and run subjacent to the A- δ nerve fibers. These are not involved with pulpodentinal complex are less easily provoked. The receptor fields for these nerve fibres are exclusively in the pulp proper

C-fiber pain is associated with tissue injury and is modulated by inflammatory mediators, vascular changes in blood volume and blood flow and increase in tissue pressure.

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POLYNODAL PAIN RECEPTORS – They respond to mechanical, thermal and chemical stimuli.

PULP PAIN Pulp pain or pulpalgia is the most commonly experienced pain in and near the oral cavity and may be classified according to the degree of severity as well as pathologic process present. DIFFERENTIAL DIAGNOSIS OF DENTAL PAIN Dental pain refers specially to pain arising from tooth pulp and / or dentine and is described as acute discomfort. When the tooth pulp is involved by traumatic injury or dental caries, inflammation stimulates pulpal noci-ceptive afferents and the underlying walls of dentin(forming the root canal)prevent swelling, so that intrapulpal pressure increases with a further augmentation of pain.

DD Hyperactive pulpalgia Dentinal hypersensitivity Hyperemia Acute pulpagia Incipient Moderate Advanced Chronic pulpalgia Barodontalgia Hyperplastic pulpitis Necrotic pulp Internal resorption Traumatic occlusion Incomplete fracture

HYPERACTIVE PULPALGIA The mildest pain discomfort experienced when no inflammation is present in hyperactive pulpalgia. It is characterized by a short, sharp shock that is due to excitation of odontoblastic cellular body with in the dentin by a noxious stimuli. It is never spontaneous ETIOLOGY It is excited by a noxious stimuli like hot or cold,sweet or sour or by touch Teeth traumatized by bruxism or incompletely fractured teeth are more hypersensitive. Brannstrom has pointed out that the displacement of tubule contents, if the movements occurs rapidly enough, may produce deformation of nerve fibres in pulp of predentin or damage to the cells. Both of these effects may be capable of producing pain. Such a mechanical transmission of stimulus would account for the great sensitivity of dentin to pain inspite of the apparent absence of nerve fibres in this tissue.

Brannstrom further confirmed the damage and pain generated by blowing air over exposed dentin. A short air blast evaporates from 0.1 to 0.3mm of fluid from the dentinal tubule. This results in immediate capillary fluid replacement from the pulps blood supply, sucking the odontoblasts and nerve fibres up into the tubule. The nerves are stretched or even torn off eliciting pain.

A- Air evaporates dentinal fluid causing rapid outflow due to capillary pressure from pulp’s vessels. B- Odontoblast and accompanying nerve fibre aspirated into tubule stretching nerve and causing pain. C- Prolonged air blast caused protein plug to form in tubule preventing outward flow

The effect of cold stimulus on the Pulp A- Cold is applied to tooth causing contraction of fluid in tubule B- Pulp capillary pressure forces replacement fluid into tubule along with odontoblast and afferent nerve. Stretching of nerve produces intense pain. DENTINAL HYPERSENSITVITY ETIOLOGY Cold food or drink or cold air. Contact of 2 dissimilar metals - galvanic shock Stimulation of exposed dentin on root surface by cold, sweet or sour substances or often just touching the surface with a finger nail or an explorer or tooth brush. It has also been reported that the use of the new calculus removing tooth pastes leads to an increased dentinal hypersensitivity.

“Sicher" postulated that the oral cavity is positively charged and the pulp is negatively charged. Any electrolyte such as salt or fruit acid upsets the ionic balance and the resultant current stimulates the nerve endings to the odontoblasts. The sensation disappears as soon as the electrolyte is diluted away,or metal is removed. According to Brannstrom concentrated solutions of sugar, salt, etc., dehydrate the tubule contents, causing their rapid outflow and deformation of nerves within the tubule. He also states that when a crack develops in dentin,as the cusp flexes with biting pressure the fluid in the tubules is pumped back and forth which stimulates pain response. HYPEREMIA It is an increased blood flow in the pulp. An increase in intrapulpal pressure against the sensory nerve endings due to heat applied on the tooth produces a sensation associated with hyperemia. This explains why the pain appears to be of a different intensity and character with application of cold or heat, the cold producing true a sharp hyperemia and a dull pain. ACUTE PULPALGIA True pulpalgia begins with the development of pulp inflammation or pulpitis. Beveridg and Brown postulated that there is an increase in intrapulpal pressure that might well be the stimulus that is applied to the sensory nerves of the pulp and leads to severe toothache. INCIPIENT ACUTE PULPALGIA The mild discomfort experienced as the anesthesia wears off following cavity preparation is a good example of incipient pulpalgia.

Stanley and Swerdlow have shown extravascular migration of inflammatory cells following even modest irritation by a controlled and cooled cavity preparation. At the incipient stage pulpitis is reversible and the discomfort vanishes. EXCITATION An irritant such as cavity preparation, cold, sugar or traumatic occlusion must stimulate incipient acute pulpalgia. EXAMINATION If the pulpalgia follows cavity preparation the involved tooth is obvious. If DC is the noxious stimulus, the cavity is found by explorer and radiographs. The lesions may be quite small first into the dentin. The patient can usually tell which quadrant is involved and may even point out the involved tooth. Cold is the best stimulus to initiate incipient acute pulpalgia. The pulp tester is of questionable value in these cases. When traumatic occlusion is causing the pain, the diagnosis becomes more difficult Moderate Acute Pulpalgia The pain of moderate acute pulpalgia is a true tooth ache but one that the patient can tolerate. The pain is frequently described as a nagging or boring pain which may at first be localized but finally becomes diffuse or referred to another area. The pain differs from that of a hyperreactive pulp in that it is not just short, uncomfortable sensation but an extended pain. The pain does not necessarily resolve when the irritant is removed, but the tooth may go on aching for minutes or hours or days.


Any act that raises the cephalic blood pressure will start the pain like the simple act of lying down. Eating something cold, starts most pain of moderate pulpalgia. Hahn and his associates have reported a co-relation between thermal sensitivity in irreversible pulpitis cases and the micro organisms- present in deep carious lesions. Using anaerobic testing methods it was found that Fusobacterium nucleatum and Actinomyces viscosus were associated with sensitivity and prolonged pain induced by cold. A warm water rinse does not usually relieve the pain and cold water makes it worse. Analgesics however bring relief. EXAMINATION Determining the involved tooth in moderate acute pulpalgia is often difficult, as the patient is unable to pinpoint the exact tooth, as the pain is widespread and vague. Examination of the suspected area may immediately reveal the involved tooth made obvious by a large carious lesion or huge restoration. Radiographs may give an immediate clue in the form of a huge interproximal cavity or a restoration impinging on the pulp chamber The involved tooth is hypersensitive and may respond sooner to the lower scale of the pulp tester but then again all the teeth in the area may respond in the same way so that no definite conclusions can be drawn from the test. Percussion and palpation rarely reveal any response although the tooth may be slightly sensitive to percussion.

The thermal evaluation is then done. cold test is used first, as the pulp is more likely to respond to this stimulus.

The tooth under the greatest suspicion is tested first by blocking the adjacent teeth with the fingers so that the melting ice does not run onto these teeth. The immediate response to cold may be quite sudden, violent and lasting. On the other hand the initial pain may go away immediately when the cold is removed. Do not test any more teeth for about 5 minutes as the pain is the tested tooth that stops acting may rebound with in a few minutes and if the dentist proceeds to test other teeth neither he nor the patient will be able to differentiate the aching tooth. If the pulp starts to ache, reapplying the cold should increase and prolong the pain. The objective is to anesthetize a single tooth at a time until the pain disappears and is localized to the specific tooth. Using either infiltration or intraligament injection, inject the most posterior tooth in the area suspected of being the cause of pain. If pain persists when the tooth has been fully anesthetized anesthetize the next tooth mesial to it and continue to do so until the pain disappears. If the source of pain cannot be determined whether in the maxillary or mandibular teeth an inferior alveolar injection should be given. Cessation of pain indicates involvement of mandibular tooth and differentiation between mandibular molars and premolars may be differentiated by the mental injection. Localization of the specific tooth is done by intraligamentary injection Advanced acute Pulpalgia The pain experienced in advanced acute pulpalgia is the most excruciating of the acute pains known to mankind.

The patient is in exquisite agony and becomes hysterical from the pain. The relief for this pain is cold water rinsed over the tooth to arrest the pain temporarily. Relief lasts for 30-45 seconds If the cold aggrevates the pain, the patient has moderate pulpalgia that might become advanced pulpalgia. EXAMINATION The involved tooth always has a closed pulp chamber. The radiograph reveals a thickened periodontal membrane space at the apex as the inflammation spreads out into the pulp. The involved tooth can be pointed out by the patient and is tender to percussion. These teeth are less sensitive to pulp tester requiring a higher reading. The heat test is the most decisive test as the inflamed pulp reacts violently to heat, hence a cold water syringe must be loaded and kept ready to provide immediate relief. When the patient is again comfortable the adjacent teeth should be tested to ascertain that no more than one tooth is involved. Local anesthesia gives blessed relief.

CHRONIC PULPALGIA In chronic pulpalgia a mild pain is present for weeks, months or years. The pain can easily be kept under control with 1 or 2 analgesic tablets 2 or 3 times daily.

Frequently the patient seeks relief only when the pulp begins to ache every night. The pain is diffuse and the patient may have difficulty locating the source of annoyance. It is also likely to cause referred pain, which is also mild. EXCITATION The pulp is not affected by cold but may ache slightly on contact with hot liquids. The patient has pain on mastication. The pain is caused by an irritant and lasts until the irritant is dislodged. BARODONTALGIA The dental pain which occurs in high altitude flying is known as barodontalgia. Its chief characteristic - being that teeth,which give no trouble on the ground under normal living conditions become excruciatingly painful at high altitudes. Coons attributed the pain to air embolism that is the presence of Nitrogen bubbles in the dental pulp. The body fluids dissolve varying quantities of nitrogen gas with varying altitudes the quantity being increased with pressure. Under normal atmosphere the body fluids dissolve about 1 litre of nitrogen. At high altitudes due to reduced barometric pressure in unpressurized cabins the nitrogen so dissolved is released and expands. The nitrogen bubbles press on the nerves and cause severe pain.

This pressure might also cause more prolonged deleterious effect on the pulp. The pain is most common in teeth with large deep seated silver fillings without underlying base materials especially in cases where teeth have been filled recently. The pain is less frequent in teeth with cement or silicate fillings and in those having defective filling margins. Severe pain occurs in teeth having degenerated gangrenous pulps and periapical disease. TRAUMATIC OCCLUSION A tooth traumatized by bruxism or a restoration in hyper occlusion often responds like the tooth with mild pulpalgia. The pulp is hypersensitive to cold and the pain is vague reminiscent of chronic pulpalgia. The tooth is not painful to mastication but there is discomfort on wakening that suggests bruxism. EXAMINATION Look for wear facets on the tooth. The mandible may also be retruded in sleep causing facets distal to masticatory facets to be involved. Examination of these should be carried out with the patient in the supine position. The involved teeth are not sensitive to percussion but are sensitive to mastication. The radiograph may show evidenced periodontal ligament space and apical external root resorption. INCOMPLETE FRACTURE Etiology

A variety of clinical situations have been correlated with cracked teeth. The following are the most commonly observed etiological factors: Teeth subjected to a traumatic incident; Teeth under heavy occlusal loads, particularly associated with tooth clenching. Heavy restored teeth with weakened transverse and triangular cusp ridges. Root-filled teeth are at increased risk. Older teeth become more brittle. Symptoms range from those of constant unexplained hypersensitive pulp to constant unexplained toothache. The tooth is uncomfortable during mastication and pain may be one quick unbearable stab. This is when the crack in the dentin suddenly spreads as the cusp separates from the remainder of the tooth. If the fracture has extended through the pulp, bacterial invasions occur and true pulpitis results. The crack may involve the crown only and present as an incomplete fracture either vertically or obliquely. An oblique fracture may be supragingival or extend subgingivally. Vertical fractures may involve the pulp and if it extends into the root will evoke acute pain. In non-vital, teeth if the crack extends to the root there will be periodontal pain and the progressive development of an infra bony pocket adjacent to the split, which may discharge into the gingival crevice with acute exacerbations. CLINICAL SIGNS

A number of clinical signs are indicative of teeth that may be split. Invariably the patient will not be able to identify the specific tooth involved, although they will be able to highlight the area in the arch where the problem is located. The patient will have developed an altered chewing pattern to avoid biting hard on particular teeth, especially with fibrous, tough or granular foods. The clinician must ask specifically about this development. There may be a history of a â&#x20AC;&#x2DC;masticatory accidentâ&#x20AC;&#x2122;, such as unexpected contact with a hard object with eating after which time the patient became aware of avoiding sensitivity in one area of the mouth. Specific sensitivity to cold such as ice applied to the tooth cusp:a small crack will result in short pain (<1 min); a larger crack will result in pain of longer duration: Cracked teeth are often insensitive to heat, unless the lesion is extensive or has been present for a long time. A heavily restored tooth crown with an underfilled occlusal surface allowing opposing tooth cusps to extend deeply into the occlusal surface and leading to a wedging effect on the already weakened tooth crown; A non-vital tooth that has been root filled and excessively instrumented; A root-filled tooth with post and core, especially where the post extends deeply into the root and mechanical preparation has removed excessive tooth structure; A root-filled tooth where the core does not incorporate a reinforcing collar to fully surround and support and prepared root face; and The presence of a deep pocket surrounding a root-filled tooth that develops acute inflammation with suppuration and discharge through the gingival crevice. It is common for the deep pocket to develop at the site of the split root only, and for the remaining gingival crevice to be of standard depth for the particular tooth. RADIOGRAPHS Radiographs may not show the crack but will indicate:

– The extent of cavity preparation and the vulnerable areas of the tooth, – The extent of root canal instrumentation, – The extent of post preparation. – The presence and location of pins. In some cases there may be a periapical radiolucency but the pathognomic sign is a unilateral radiolucency along the lateral aspect of the root adjacent to the fracture. PERIRADICULAR PAIN ACUTE PERIAPICAL PERIODONTITIS SYMPTOMS This acute form is pain is the most excruciating of pain and lasts for days. The tooth is equisitely painful to touch and even contacting the tooth in closure may bring a flood of tears. The pain is most persistent lasting 24hours of the day. The pain has been described as a constant, gnawing, throbbing and providing. Eventually the pain may gain relief only to bite on the tooth that starts the pain cycle once more. Even if the tooth is extracted the pain continues for another 48 hours owing to osteitis. ETIOLOGY The irritants introduced during root canal therapy by the clinician perforating the root apex forces caustic medicaments or irritating solution through the apical foramen or forcibly deposits necrotic, infected and toxic canal contents into the periradicular tissue which produces a violent inflammatory reaction. If the bacteria are present in the canal and are extruded apically an acute abscess also develops to complicate the picture. Typically acute apical periodontitis follows initial endodontic treatment.

The increase in pain is due to the small amount of cancellous bone and the thick bony cortex found in the area of mandibular teeth limits the space allowable for swelling. EXAMINATION The tooth is in supra occlusion and the mandible cannot be closed without initial impact on the involved tooth. ACUTE APICAL ABSCESS The pain of acute apical abscess is of lower intensity than acute apical periodontitis. Necrosis of the acute abscess destroys enough tissue to permit fluid dispersement. The extravasated fluid breaks out into the soft tissue and marrow spaces where the swelling is not confined. A systolic throbbing pain is present on palpation. The involved tooth is also painful on mastication. ETIOLOGY The abscess develops due to the bacterial invasion of the periradicular region from the necrotic pulp canal. It may also develop from a pulpless tooth or may follow initial endodontic treatment if bacteria are forced into the periradicular tissue. The initial discomfort is mild but gradually builds in intensity as the abscess becomes indurated or hardened. When the alveolar plate is "erodedâ&#x20AC;&#x153; by the process and the abscess gathers into frank pus, the entire area softens and feels fluctuant to palpation and the pain is greatly reduced. EXAMINATION The degree varies from initial undetected swelling to gross cellulitis and massive asymmetry. The involved tooth is painful to percussion or palpation.

Radiographically, the periodontal space may be widened or a large alveolar radiolucency is present. Electric pulp testing shows that the pulp is necrotic. The vitality test differentiates acute apical abscess from acute periodontal abscess. In the case of periodontal abscess the pulp is not necrotic and on percussion the teeth is not so painful as the abscess is found on the side of the root. On the other hand percussion against inflamed periapex in acute apical abscess causes great increase in pressure due to the wedging effect of the tapering root. Heat test may increase the pain momentarily due to increase in gas expansion in the area. Cold may give slight relief. PERIODONTAL LESION PAIN Few periodontal lesions are severely painful. The causes of these lesions are divided into diseases that attack just the gingiva and those that involve the deeper periodontal complex. Two uncomfortable lesions that involve the gingiva and mucosa are acute nectrotizing ulcerative gingivitis and herpes simplex. These disease offer no severe problems in the differential diagnosis of pain, because both lesions are diagnosed from their appearance and / or odour.

Two painful conditions that involve the pericemental structures, and must be differentiated, are the acute gingival or periodontal abscess and periocoronitis. Acute Gingival or periodontal abscess The patient with an acute periodontal abscess seeks treatment for a tooth that is painful to move or to bite on. The pain, however, is not so deep seated or so throbbing as that of an acute apical abscess. Although some localized swelling is present, it is not so extensive.

ETIOLOGY It develops from a virulent infection of an existing periodontal pocket or as an apical extension of infection from a gingival pocket. Most gingival abscesses are associated with traumatic injury to the gingiva or periodontium by a mechanical force. Both types of abscess are frequently seen in patients who have compulsive clenching or bruxism. EXAMINATION The periodontal abscess “points” opposite the coronal third of the root, whereas the apical abscess generally “points” opposite the apex. The electric pulp tester is the surest method of differentiation. The necrotic, infected pulp causing an apical abscess always gives an essentially negative response to testing, whereas the tooth involved with the periodontal abscess is generally vital. Use of the periodontal probe often reveals a tract from the gingival sulcus to the abscess.

PERICORONITIS The common complaint of the patient with pericoronitis is severe radiating pain in the posterior mouth and the inability to comfortably open or close the mandible. The tissue distal to the erupting molar is most painful to touch, especially during eating. The pain radiates through the region, down into the neck, and up into the ear, and can easily be confused with pulp pain. ETIOLOGY

It is caused by injury and infection of the pericoronal tissues associated with erupting molars, usually mandibular third molars. EXAMINATION The history of trismus and discomfort on opening or closing the mandible is indicative of periocoronitis. When the operculum is palpated or probed, it is found to be swollen and exquisitely painful. PREVENTION OF PAIN The main methods of preventing pain are determined by the mechanisms of development and transmission of pain. CONCLUSION Pain is one of the most common symptoms for which patients seek treatment, and managing pain and relieving suffering should be at the core of the health professionals commitment to patients.

Pathophysiology of pain/ dental implant courses by Indian dental academy