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Historical Note  Pain has a long date back to the earliest civilizations.  Homer described pain as arrows shot by the Gods  Aristotle said that pain was a passion of the soul  Plato the student of Aristotle said that pain was an emotional experience Def of Pain Pain is a perfect misery, the worst of all evils and if excessive overturns all patience Pain can be defined as a more or less localised sensation of discomfort, distress or agony resulting from stimulus of speacialized nerve endings ( Dorlands Medical Disctionary) Acc to Field Pain is an unpleasant sensation that is perceived as arising form a specific region of the body and is commonly produced by process that damage or are capable of damaging bodily tissues. According to international Association for study of pain An impleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.

Pain is always subjective. Each individual learn the application of the work through experience related to injury in early life. II. REFERRED PAIN Pain arising from deep tissues, muscles, ligaments, joint and viscera is often perceived at a distant site from the actual nociceptive source. Pain of angina pectoris ďƒ Left arm / Jaw Diapharamatic Pain ďƒ  Shoulder / Neck Cutaneous pain is sharp burning and clearly localized. Referred pain on the other hand is fromthe muscle. It is often diagnostic dilemma. 2 MOST POPULAR THEORIES 1. Convergenate Projection Theory Most popular Theory Primary afferent nociceptiors from both visceral and cutaneious neurons converge onto the same second order pain transmission neuron in the spinal cord. Multiple sources include Vth , VIIth IXth and XIth Cranial nevers and cervical plexus a C2 and C3 that is pain information from the face, teeth, TMJ ear, pharynx larynx , scalp and other associated structures is

converging into a pool of nociceptive neurons located at the branstem level ďƒ sub nucleus caudlis of spinal nucleus. CONVERGENCE FACILITATION THEORY 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 be increase or be facilitated. Facilitation from the deeper nociceptive impulses causes the pain to be perceived in the area that creates the normal resting background activity. CLINICAL OBSERVATION : Blocking sensory input from reference area with either LA or Cold can sometimes reduce the perceived pain. ACCORDING TO MENSE : Convergent connection from other spinal cord segments are unmassed or opened by noiceptive input from the skeletal muscle. Leading authors produced tooth ache by placing stimulating electrodes into the defects in enamel of their own teeth. They found that delivering upto 10 .0 volts to teeth, severe pain could be induced .

Systematically they mapped and described the reference pain from a number of teeth , mandibular and maxillary teeth alive. III. NERVE SUPPLY TO JAWS The trigeminal nerve the largest cranial nerve contains both sensory and motor nerve and is the principal nerve supply to face. Opthalmic, maxillary and mandibular divisions from the peripheral branches of trigeminal nerve. IV. PAIN PATHWAYS 3 of many theories to explain pain transmission are ; 1) specificity theory 2) pattern theory 3) Gate control theory 1) SPECIFICITY THEORY (By Von Frey) Different sensory fibers mediate different sensory modalities ďƒ Pain, heat, cold touch, pressure. Receptors for pain or unmyelinated free nerve ending and are mostly specific. 2) PATTERN THEORY Pain generated by non specific receptors. Assumes that all nerve fibre endings and that pattern for pain is produced by more intense a stimulation than for other simulation .

3) GATE CONTROL THEORY (By Melzack and Wal) 2 factors that control gate theory a) Gating mechanism b) descending central control from intrinsic brain mechanism.

Fibers A (α) A ( β) A (γ) A(δ) B C

Diameter µm 13-20 6-13 3-8 1-5 1-3 0.4-1.0

Velocity m/sec. 70-120 40-70 15-40 2-30 3-15 0.4-2

Function Touch pressure and proprioception Pain and temp Pain and temp Efferent for pain “ “

Clinical application of gate control 1) Higher center modulation 2) Spontaneous intermittent and continuous pain Alternate A (β) & C fibers stimulation as a result of pulp inflammation close and open the gate thus explaining the intermittent and spontaneous pain.


Exciting Factors : Cold food , cold air, contact of 2 dissimilar metals, vegetable or fruit acid, salt or glycerin , touching surface with a interdental stimulators, finger nail filing enamel exposes . Uses of calculus removing tooth paste. Following pole surgery Explanation : Brannstrom Hydrodynamic theory A short blast of air evaporate 0.1 – 0.3 mm of fluid from the dentinal tubule. This results in immediate capillary fluid replacement from the pulp, blood supply sucking the odontoblasts and nerve fibers up with the tubule. The nerve is stretched and even tooth off resulting in pan continued exposure – protein play. b) Hyperemia Capillary

bed engagement with the predisposition to edema.

Increase in intra pulp premier produced by HEAT 1. Heat produces  Transient hyperemic and dull pain 2. Cold produces  Sharp hypersensitivity Cold stimulate fast conducting myelenated A Fibers heat application slow conducting non myelinated C fibers. Pulp pan causes first fall and then when stimulate removed nice in pressure.


Isolating tooth and checking for cold test

Recent restoration  Response to application of cold

More sensitive to EPT (time linc, hot sharp or warm)

AB fibers  EPT

Aδ fibers – stimulated by tubule fluid movement

Aδ fibers – stimulated by tubule fluid movement at higher levels of EPT  A + C (Stimulation ) Produces the painful response (C = fibers “Kick in “ ) TREATMENT Physiology Modality Remineralization of dental tubular from the calcium phosphate carbohydrate protein complex. CHEMICAL / MECHANICAL a) Potassium Oxalate (BY Green with and Pashley) (PROTECT) b) Stontium chlorides SENSODYNE THEMODENT tooth paste

Strontium combines with phosphate and exchange for Ca in the hydroxyapatite apatite of the dental tubule productivity strontium phosphate crystals and have dentinal tubular closure. According to GOOD MAN Strontium alter the neural transmission hence







hypersensitivity. C) Fluoride Iontophoresis Popularized by GANGEROSA Using 1 to NaF is the method of choice. Singl application is sufficient d) Potassium Nitrate (by HODSH) PROMOTE SENSODYNE Reducer the sensitivity of the mechanoreceptors Nerve to the movement of dentinal fluid c) Scotchbond d) 4 META



Minor to moderate inflammatory condition of the pulp caused by noxious stimuli in which the pulp is capable of returning to the uninflammed state following removal of stimuli.

Incipient Acute pulpalgia Stimulated by cavity preparation, cold, lesion may be small just into dentin cold in the best stimulus .

Removal of common lesion

followed by Ca (OH)2 application and sedative cement. HISTOPATHOLOGY 

Hyperemia to mild moderate inflammation change in the involved of dentinal tubule

Reparative dentin

Disruption of orthodontic procedure

Ditated blood vessels

Extravasation of edema fluid

Presence of immunologicalluy competent chronic inflammatory cells.


Sharp pain lashing a movement with COLD

Does not occur spontaneously



Early insertion of a filling if a cavity her developed

Once stimulus removed tooth should be tested for pulpal necrosis

IRREVERSIBLE PULPITIS Persistent inflammatory condition of the pulp caused by noxious stimuli. Pain occurs spontaneously. Lasts for several minutes to hours lingering often after removal of thermal stimuli HISTOPATHOLOGY Caries Chronic inflammation Congestion of post capillary vessels Necrosis Attract PMN Release of Lysosomal enzyme Micro abscess Early rise in intrapulpal presence will cause a spontaneous throbbing pain done by pulsating of intra pulpal pressure.

As the intra pulpal pressure increases and becomes supratheshold – pain in felt as spontaneous constant pain. Predentin may be reduced in width (absent after removal of stimuli pain lasts. This is done to secondary initiation by the injured and dead cells and later the produce of proteolysis 

When acute symptom such as pain and swelling level inflammation is basically chronic but acute inflammatory response may be over laid or a chronic lesion .

When pulp exposure result from dental caries pulp has been chronically inflamed for a long time.

Development of painful symptoms is due to blockage of canal orifice through which the exudate drains.

Suppurative 2 Nos is (Zone I ) evident and referred to zone of necrosis / inficlior.

Zone II is the inflamed connective tissue core surrounding the core.

An inflammation persist to until all derived at the outer zone III and IV (Zone of institutor and Zone of stimulation )

Diagnosis Patient feels a throbbing sensation (pulp wave stimulatory of c fibers) - Pain is spontaneous - Varying posture can stimulate pain, hot food or drink sucking milk cavity, biting food into cavity - Pain triggers after removal of stimulus - Patient may locate the general area of discomfort but cannot pinpoint the tooth . RADIOGRAPHS : Periapical is usually normal widening of pdl space with tenderness to percussion. Acute pulpitis with acute apical periodontitis Widening of PDL space with out tenderness to percussion ďƒ Acute Pulpitis with chronic apical periodontitis -

Hyper responsive to thermal stimuli


Pain persists after removal of stimuli

Cold does not initiate pain to as the peripheral A S fibers in the miner dentin or the dentinoblastic and subdentinoblastic zones are no longer viable and the therefore inceptable of transmitting . action potentials.

E & T not of a diagnostic value is acute advanced cases of multirooted teeth. TREATMENT : RCT CHRONIC PULPITIS 

Inflammatory response to a pulpal irritant

Pain is absent due to diminished oxidative inflammatory actively and a corresponding decreases in the intrapulpal pressure.

Discomfort best describe as GRUMBLE

Can withstand pain for weeks, mouth, years

Vague pain

Not excited by cold but may ache slightly on application of hot liquids.

Can be classified as (According to WEINE) Chronic Pulpitis Hyperplastic (Ulcervative or Pulp Polyp open form) Formulation

Closed Forms Trauma

Extensive carious lesion of of young pulp


abscess at site of H / Po covered by stratified exposure (ulcer )

squamous epithetic Ortho movement Symptoms less except during mastication when pressures of food







leave with scar of denticles,

discomfort diffuse calcification and Non sensitive than gingival increased irritation dentin tissue all of which diminish and Fleshy , Reddish , pulp mass Bleeds due to rich network of obstruct lumen of pulp blood vessels chamber and canal More than normal current for EPT Differentialied from gingival polyp

PULP NECROSIS Sequence of acute and chronic inflammation of pulp or an immediate arrest of circulation by traumatic injury.

2 Types of necrosis  liquefaction Necrosis  Coagulation necrosis Coagulation Necrosis : Diminishing or cutting of blood supply. First can have appearance of soft solid mass. Cheesy consistency . Tomb stone appearance. Liquefaction Necrosis : Complete destruction of cell mass. Decomposition of protein by anaerobic bacteria and termed – PUTREFACTION .  Pain is absent  No response to vitality tests  Definite color change due to altered coronal translucency. INTERNAL RESORPTION  Affected pulp is completely free of symptoms  Mimic moderate acute pulpalgia  Pink tooth appearance  Painful only to pressures on mastication .




Increase with age

Deposition of Ca +ve in dead


Fibrosis (increases collagen)

and degenerating tissues.


cells appear as sunken


Solid particles in use of dense fibers


Pyknote nuclic of fibroblasts


Crab Grass appearance IV.

Pain disorders the Mimic odontology

Typical Periodontologia



Reflex sympathetic dystrophy


A typical facial pain


Phantom tooth pain


Neverlgia inducing


Cavitational induced Osteonecrosis

Salivary gland (Glandular) Musculoskeletal Meoplastic


PERIODONTALGIA Periodontal pain complaints are often expressed as a localized deep pain and may involve periodontal tissues around one or more teeth . Soft tissue infection or inflammation or both (e.g. swelling, redness, tissue sensitivity) is often associated with this disorder. Associated teeth are often sensitive to temperature and pressure and may feel elongated. Dental mobility may also be observed. Often examination will disclose localized bleeding and measurable pocket depth, and radiographs will reflect loss of supporting alveolar bone. When periodontal pain involves multiple teeth, including opposing teeth, occlusal trauma should be considered. This should include traumatic effects, dental malocclusion , and bruxing and clenching.

In many instances, periodontalgia and

odontalgia may coexist and involve multiple tissues. NEURALGIAS The pain involves one or more of the trigeminal nerve divisions and, although the precise cause is known , empiric evidence suggests that the symptoms evolve as a consequence of vascular compression of the Gasserian ganglion. Two highly characteristic features of tic douloureux allow into be differentiated from other facial pain syndrome.

The character and

duration of the symptoms are unique, and a specific anatomic trigger

point can be identified. Although the pain may sometimes involve the ophthalmic division, is primarily involves either the maxillary or the mandibular division.

In addition the pain is severe and lancinating,

shooting into the bone and teeth. Trigger area may be one 2 mm wide. POSTHERPETIC NEURRAGIA Primary infection with varicella zoster virus (VZV) causes chickenpox, a disease that affects over 95% of the population during early childhood. This disease represents a recrudescence of a latent virus located in sensory ganglia. Vesicles terminate at the midline and involve only one division of the trigeminal nerve. The painful lesions of shingles cause a deep, boring ache, involving not only the superficial mucosa and cutaneous tissues but also the maxillary or mandibular bones. Before the onset of the vesicular eruption, it is common for the patient to experience prodromal pain, obscuring the diagnosis . These prodromal symptoms frequently simulate trigeminal neuralgia: They last only seconds and have an electric – like quality.

Patients show clearing of vesicles in less than 5% of varicella zoster infections , and pain is likely to persist. In addition, postherepetic neuralgia may persist weeks, months, or years. The prodromal pain is acute and electric like, and the pain associated with vesicular eruption is deep and boring However, once the vesicles clear, the residual pain has a burning quality and is chronic. Occasionally deeper achieving pains may be assoiated with this burning element, suggesting pain of odontogenic origin. VASOGENIC CRANIOFACIAL PAIN Cluster headache is often mistaken for acute pulpitis or apical abscess of a posterior maxillary tooth. The pain frequently occurs just after the patient retires and is entering the early stages of rapid eye movement (REM) sleep . The onset is acute and severe with patients indicating that it feels like a hot poker has been jammed into the upper jaw and behind the eye. Typically, the pain continues to increase in severity and persists for 30-45 minutes. Another form of cluster headache is referred to as chronic cluster. These headaches are similar to the classic form in that they occur on an episodic basis and typically last 30 to 45 minutes. However, chronic cluster headaches after the patient year round, rather than seasonally.

The current therapy for cluster headache uses vasoactive drugs, particularly the calcium channel blockers. When prescribed on a regular basis, nifedipine (or one of its related compounds) prevents the pain paroxysms and is of benefit for both classic and chronic cluster headache. In addition , prednisone (i9n combination with lithium) has been shown to be effective in alleviating to preventing to pain of cluster head ache. Hyperbaric oxygen therapy has also been sho0wn to have preventive effects.

In addition the vasoactive antimigraine drug sumatriptin

succinate a 5-hydroxytryptamine receptor against that is administered subcutaneously, is effective for treatment of cluster headache. However, oral administration of this drug is not particularly beneficial. TEMPORAL ARTERITIS. Also known as giant cell arteritis, temporal arteritis is a granulomatous inflammatory disease of the temporal artery wall in which the vessel wall is thickened and inflamed. Temporal arteritis causes throbbing pain in the temple region. The disease usually appears in late life, and the temporal artery is often visibly thickened with erythema of the over lying facial skin.

The sedimentation rate is elevated, and

laboratory tests assist in confirming the diagnosis. Biopsy is also a means for diagnostic confirmation, because giant cells and granulomatous inflammation can be identified in the adventitia of the artery. Temporal

arteritis can involve other carotid branches, including the facial artery, creating pain symptoms that may be experienced in the maxilla, mimicking toothache. OTITIS MEDIA Infection of the middle ear is common, particularly in children and is caused by pyogenic microorganisms. Middle ear infections may be confused with odontogenic pain because the symptoms radiate from the ear over the posterior aspect of the maxilla and mandible. It would be unlikely for middle ear infection to be exclusively expressed as jaw pain. The nature of the pain is acute; patients complain of a severe ache, and throbbing is a frequent accompaniment. Gravitational factors may also come into play; pain is often exacerbated as the patient lower the head. The pathogenesis is straightforward and is, in many ways similar to that of acute pulp pain. In the dental pulp the noxious components of the inflammatory








microorganisms accumulate in a confined space. The definitive diagnosis is made by using an otoscope to examine the tympanic membrane, which is usually red and bulging. Treatment consists of antibiotic therapy, usually pencillin with P – lactase inhibitor

or clindamycin, occasionally syringotomy is necessary.

Once the

diagnosis is established, referral to an otolaryngologist is recommended. ALLERGIC SINUS : Allergies tend to be seasonal, because most people with upper airways allergic reactions respond to various seeds and pollens. IN northern climates the prevalence of sinusitis increases in spring and fall. The contact of an allergen with the Sino nasal mucous membrane results in an immediate – type hypersensitivity reaction that is mediated by an antigen that generates the respiratory epithelium, enters the submucosa, and is bound to an immunoglobulin E antibody. Involvement of the sinus includes mucosal thickening and the presence of a fluid level within the maxillary sinus cavity. Frequently the posterior maxillary teeth seem to itch and the patient feels completed to clench. Percussion sensitivity is evident on all of the molar teeth, and frequently the premolars are percussion sensitive as well. This sensitivity is not acute; rather, it is experienced as a dull discomfort. As with acute sinusitis, symptoms may be accentuated by having the patient place the head between the knees.

The diagnosis is supplemented by antral transllumination, in which light will not illuminate an affected maxilla in a darkened f\rooms. Waters sinus radiographs will discolose either soft tissue membrane thickening of the antral walls or an air fluid level will be discernable . Mucosal changes are also evident on MRI and CT scans. Decongestants and nasal sprays, along with antihistamines, are the treatment of choice. Identification of the allergen and desensitization may offer relief for some of patients and referral to an otolaryngologist or an allergist should be considered.

Angina pectoris : The most common manifestation of coronary vascular occlusion, particularly in its acute manifestation, is substernal pain with referred 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. Specifically, electrocardiography or stress test may be advisable. Treatment consists of a variety of intervention, including restricted intake of lipids administration of aspirin to prevent thrombosis, and surgical intervention by coronary angioplasty or bypass surgery should angiography show significant occlusive disease. SIALOLITHAISIS Unlike kidney stones and gallstones, sialotliths are unrelated to increased levels. Of serum calcium or to dietary factors. Desquamated epithelial cells from the major salivary ducts may accumulate and form complexes with salivary mucin to form a nidus for calcification. 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 o the submandibular area. Hence it may mimic lymphadentis associated with an endodontic infection of a posterior mandibular tooth.

Pain is exacerbated by salivation (induced by a lemon drop a mealtimes) the floor of the mouth can be palpated using a milking motion. When the major duct is occluded, no saliva will flow from the duct orifice. The nature of the pain is also revealing in that the patient feels a stringent drawing in the area. Occlusal radiograph will disclose the presence of a soft tissue calcification along the course of the duct in the floor of the mouth. It should be noted that panoramic radiographs may reveal an opacity in the mandible. In such instances the soft tissue calcification is simply superimposed (although it may mimic facial sclerosing osteomyelitis. Treatment consists of physical attempts to remove the stone by manipulating it out the orifice. Larger stones cannot be removed in this fashion and will require a surgical cut down to the duct. ABNORMAL JOINT FUCTION (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.

It has been proposed that stress-related jaw clenching and bruxism may place stress on the meniscus and causes anterior displacement. Alternatively traumatic events (e.g. motor vehicle accidents), yawning, and prolonged jaw opening have bee suggested to cause compression or overextension of the ligaments, with secondary displacement of the meniscus. 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 dull , boring ache, but it may be more acute when exacerbated by wide opening of the mandible of chewing. ATYPICAL PAIN DISORDERS THAT MIMIC ODONTALGIA Of all the facial pain syndromes, the group that most often simulates endodontic or odontogenic pain is “atypical facial pain� . 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. Although psychologic actors have been suggested to be important in phantom tooth pain, there is not a great deal of evidence.. NEURALGIA – INDUCING CAVITATIONAL OSTEONECROSIS (NICO) Neuralgia – inducing cavitational osteonecrosis (NICO) is an atypical orofacial pain localized to edentulous foci, which can sometimes be alleviated with a subperiosteal injection of local anaesthetic. In such instances it has been proposed that small residual inflammatory foci exist within the endosteum, and that 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. The validity of this theory of atypical facial pain arising in edentulous region is not universally accepted and is considered somewhat controversial. CAUSALGIA Causalgia pain can involve the jaws, head, and neck.


present, it may be confused with odontalgia. T is often associated with trauma, jaws, fracture, or laceration and it may evolve after surgery. 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. Whether atypical facial paints lie in edentulous areas, are poorly localized or are centered in teeth treatment should be approached cautiously.

CONCLUSION As it is and will emphasized the proper diagnosis of pain can lead us to diseased that were not noticed earlier. Hence a quantification of knowledge and with the knowledge of the above presented disorders our diagnostic view is open and magnified and we can

rule out more

possibilities. But still we have to be on the look out of those lesions that have no clue.

REFERENCES 1) Pathways of the Pulp - Cohen 2) Endodontics – Ingle 3) Endodontic therapy- Weine 4) Orofacial Pain - Bell

Orofacial pain mimicking pain of endodontic origin/ dental implant courses by Indian dental academy  
Orofacial pain mimicking pain of endodontic origin/ dental implant courses by Indian dental academy  

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