Toothache of Cardiac Origin

Marcelo Kreiner, DDSAssistant ProfessorDepartment of General and Oral

PhysiologyFaculty of OdontologyUniversity of UruguayMontevideo. Uruguay

Head, Orofacial Pain AreaUruguayan Society of StomatoiogyUruguayan Dental AssociationMontevideo, Uruguay

Jeffrey P. Okeson, DMDProfessor and DirectorOrofacial Pain CenterUniversity of Kentucky College of

DentistryLexington, Kentucky

Correspondence to:Dr Marcelo KreinerRamon Masini 3381 ap 601Montevideo 11300UnjguayFax: 598 2 9012860E-mail: mkreiner@netgate.com.uy

Pain referred to the orofacial structures can sometimes be a diag-nostic challenge for the clinician. In some instances, a patient maycomplain of' tooth pain that is completely unrelated to any dentalsource. This poses a diagnostic and therapeutic problem for thedentist. Cardiac pain most commonly radiates to the left arm,shoulder, neck, and face. !n rare instances, angina pectoris maypresent as dental pain. When this occurs, an improper diagnosisfrequently leads to unnecessary dental treatment or, more signifi-cantly, a delay of proper treatment. This delay may result in thepatient experiencing an acute myocardial infarction, it is the den-tist's responsibility to establish a proper diagnosis so that thetreatment wilt be directed toward the source of pain and not to thesite of pain. Tbis article reviews the literature concerning referredpain of cardiac origin and presents a case report of toothache ofcardiac origin.J OROFAC PAIN 19

Key words: cardiac pain, referred pain, nonodontogenictoothache, hererotopic pain, orofacial pain

Many different types of pain disorders are feir in the orofa-cial structures. The clinician managing orofacial painmust always be aware of the many possibilities so that a

proper diagnosis is established. Too often an improper diagnosisleads to ineffective and unnecessary therapy. This is the greatestchallenge for the clinician. One of the most common pain com-plaints routinely seen in the dental office is toothache. Toothachesof dental origin, such as pulpal and periodontal, are routinelymanaged well in the dental office. Some toothaches, however, arenonodontogenic, meaning that although the patient reports pain intbe tooth, the actual source is not dental but instead originatesfrom another location. These types of pains are called heterotopicpains. Heterotopic pains need to be identified before treatment isbegun, since the success of a therapy depends upon bearing thetrue source of the pain, not the site of the pain. One possiblesource of heterotoptc toothache is cardiac pain. This type of painneeds to be identified tmmediately, not only to avotd tnapproprt-ate dental therapy, hut also to ensure that the patient is referred tothe proper health care professtonal for appropriate therapy. Thispaper will highlight the pathophysiology oí cardiac patn referraland the clintcal presentation of toothache of cardiac origin.

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The Pathophysiology of Cardiac Pain

In recent years, researchers bave tried to betterunderstand the origin and mechanisms that under-lie cardiac pain, such as angina pectoris, and thecommon complaints of associated pain referral.The contribucions of cardiac nociceptors, chemicalmediators, afferenc pathways, and central neuralmechanisms are some of the most imporCanC topicsthat have been investigated. Although che underly-ing mechanisms of cardiac pain are still poorlyunderstood, most data suggest that ischemia of theheart muscle is the main cause of cardiac pain,'"^In experimental conditions, coronary artery occlu-sion activates cardiac afferent nerves.''"*' Theperipheral biochemical changes that occur duringcardiac ischemia include alterations in tissue con-centrations of hradykinin, serotonin, adenosine,porassium, and prostaglandins.^"'^

It is still unknown which specific chemical medi-ators released during coronary occlusion areresponsible for evoking painful sensations.Attempts Co idencify a single mediator causingnociceptive stimulacion have failed ;̂ therefore, it islikely chat multiple nociceptive mediators atereleased simultaneously. Bradykinin is believed tobe tbe most important mediator of cardiacpain.'- ' ' ' Veelken et al̂ "" showed that cardiacbradykinin elicits a sympathoexcitatory reflex,supporting rhe idea that this chemical mediatormay increase sympathetic activity during cardiacischemia. It is interesting to note that bradykininalone does not produce pain in experimental ani-mals,^^"'̂ suggesting that it may play only a sup-portive role in cardiac pain.

Serotonin has also been studied as an importantchemical mediator of cardiac pain. Intracoronaryinjeccions of serotonin in lightly anesthetized dogscause pseudo-affective responses indicative ofpain,-'̂ ^ Serotonin blood concencracions increaseafter experimental coronary occlusion or afterangina attacks,^^ suggesting its involvement as amediator of cardiac pain. There is evidence thatadenosine is also a mediator in angina. Coronarysinus concentrations of adenosine are elevated fol-lowing myocardial ischemia, and after intravenousadministration of adenosine, angina pectoris-Iikepain was reporced in healthy volunteers.^''•^' Theexiscing data suggest that this mediator can sensi-tize afferent cardiac nerves during painful cardiacischemia.̂ ^ Potassium has also been shown to par-ticipate in angina peccoris mechanisms. Extra-cellular potassium concentration in myocardial tis-sue increases rapidly after cardiac ischemia,^'However, the potassium release is often within

physiologic ranges during ischemia and may not besufficient to induce angina.

It is widely accepted that the pathway of cardiacnociception produced by ischemia is by way of thecardiac sympathetic afferent system.̂ ''"-^ However,the idea that only sympathetic fibers are responsi-ble for this transmission has been challenged hyseveral reports. These studies have shown chaconly 50 to 60% of patients who underwent sym-pathectomy reported complete relief from anginapectoris, wbile 40% tepotted partial relief and 10to 20% reported no relief at all.^

Vagal afferent involvement in pain transmissionfrom the ischémie heart is not clear, but a reviewof clinical and experimental reports^^"^^ suggeststhat it can play an important role. After considera-tion of tbe anatomic distribución of the sympa-thetic and vagal fibers, it has been speculated thatangina may be primarily the result of sympatheticafferent activation in the anterior surface of theheart, while vagal afferent could be activated onthe inferior-posted or surface,'

Angina pain is a common clinical manifestationof coronary disease. Myocardial ischemia, how-ever, should not be considered synonymous withangina pectoris.̂ "^ More than 25% of myocardialinfarctions may be asymptomatic, and in somecases "silent" infarctions are detected only bypathologic findings on a routine electrocardiogram(EKCi).^' Pacients who experience "non-silent"acure myocardial ischemia may present with avariecy of clinical symptoms.

Cardiac Pain Referral

The central processing of nociception arising fromthe heart during iscbemia involves complex mecha-nisms. Several reports have shown that cardiacafférents and somatic inputs from tbe upper limhs,chest, and face converge on spinothalamic tractneurons in the central nervous system (CNS).̂ '̂̂ -̂̂ ^Convergence mechanisms and central sensitizationin the trigeminal complex have also been suggestedas an explanation for the referral of pain to tbeorofacial structures (Fig 1). As cardiac nociceptiveinput enters tbe CNS and ascends to the highercenters for evaluación and interpretation, adjacentcentral neurons in the tegion of convergence canalso become activated. This results in rbe stimula-tion of these adjacent nociceptive neurons, whichare not directly involved wich the primary sourceof pain. As the information ascends, the cortex canmisinterpret chis data as pain in another site (bet-erotopic pain). Thus, pain can be felc in the region

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Pain

Fig 1 This figure simplistically illustrates a possible mechanism responsible for pain

primary source of the nociception is the cardiac muscle (primary pain). CN - cranialnerve. Adapted from Okeson^^P^- with permission of the publisher.

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of the mandible secondary to cardiac ischemia.More specifically, as depicted in this article, paincan actually be felt in the region of a tooth whenthe primary source of nociception is the cardiacmuscle.

Deep pain input from visceral structures hasbeen demonstrated to converge in specific laminaof the dorsal born and trigeminal spinal tractnucleus, with other primary afferent neurons car-rying input from trigeminal structures.'•* This con-vergence of input leads to the possibility that noci-ceptive input from visceral structures, such as theheart, can lead to pain referral in the trigeminalregion.

There is still scientific debate regarding theperipheral and central neural mechanisms involvedin referred pain arising from the heart.Sympathetic fibers are clearly involved, but therole of the para sympathetic system is not as clear.Cardiac inputs enter the CNS through the spinalcord and terminate mainly in the thoracic dorsalhorn, where they synapse with spinothalamic tractneurons. Tbe information is then pro|ected to thethalamus. Convergence mechanisms into thetrigeminal brain stem complex and/or in the thala-mus can explain referred pain to the face. In angi-nai occipital headache, it has been proposed thatthoracic input ascends via Lissauer's tract to con-verge with tbe upper cervical inpur.-''

Cardiac pain can be referred to the trigeminalregion without tbe typical clinical presentation ofangina pectoris. In some rare instances, jaw and/ortooth pain can be the only clinical complaint. Inthese situations it is the dentist's responsibility toestablish the appropriate diagnosis and immedi-ately refer the patient to the appropriate healthcare professional.

Clinical Characteristics of Cardiac PainReferred to the Orofacial Structures

The clinician should always assess the patient'spain complaint by evaluating the pain location andits quality, intensity, and duration. The clinicianshould also consider any aggravating, relieving,and radiating factors.^^ Typically, cardiac pain islocalized in the sternal region and left side of thechest. The pain can frequently radiate to the neck,left arm, shoulder, jaw, teeth, eyes, and head.̂ '-^*

The duration of the attack can vary from a fewminutes to 1 or 2 hours. The primary precipitatingfactor is usually physical effort, but the patientmay not associate the pain with any cardiacsource. Rest and sublingual nitroglycerin tablets

are the most common relieving factors." The pres-ence and intensity of pain are variable and do notindicate different levels of the disease. In fact, thecardiac hemodynamic and mechanical changesexperienced by individual patients during bothsymptomatic and asymptomatic episodes can bequite similar.'^

Several reports"'"^' bave demonstrated a clinicalrelationship between cardiac ischemia and orofa-cial pain. Toothache, mandibular pain, ear pain,and beadache are the most commonly relatedsymptoms, Tzukert et al'*" reported 3 cases inwhich orofacial pain was the initial chief com-plaint. A 56-year-old woman complained of bilat-eral sharp pain in the anterior maxillary area thatradiated to the infraorbital region, neck, and shoul-der. Clinical examination sbowed no evidence oforal or dental pathology. Marked dyspnea alertedthe clinician to the possibility of cardiovascularinvolvement, and the patient was referred to a car-diologist. During a stress test, the patient devel-oped the facial pain complaint associated withEKG abnormalities. Coronary obstruction wasdemonstrated witb an artériographie examination.A coronary bypass procedure was performed, andthe facial pain complaint was resolved.

The second patient reported by Tzukert was a7.9-year-old man who complained of severe pain inthe jaw. The clinical history also revealed episodesof chest pam. The facial pam responded immedi-ately to sublingual administration of isosorbidedinitrate. An EKG sbowed evidence of acuteinferolateral myocardial infarction. Tbe last casewas tbat of a é7-year-old man witb bilateralparoxysmal jaw pain. The pain was associatedwith physical effort. It usually appeared when hewalked back to work after lunch. The patientdescribed no otber complaints, and no source offacial pain was identified. A cardiologist treatedthe patient with propanolol and nitrites, whichresolved ali facial pain symptoms.

Batcbelder et aH^ reported a case of anginal painlimited to the mandible, in which a misdiagnosisresulted in unnecessary dental treatment and adelay in appropriate management. This was a 71-year-old male who complained to his dentist ofdental pain. The pain was initially diagnosed asodontogenic, secondary to pulp disease in amandibular first premolar. Endodontic treatmentwas performed, but the pain did not resolve. Thepatient was then referred for diagnostic consulta-tion, which revealed a history of chest pain andpossible cardiac involvement. Tbe patient alsoreported left shoulder and clavicular region painthat was relieved hy rest. An EKG showed severe

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injury to the anterior wall and ischemia whencompared with an EKG taken 1 year earlier.Coronary angiography showed 90% occlusion ofthe left anterior descending coronary artery. Thepatient reported that nitroglycerin medication tookaway the pain.

In a report by Penarocha Diago et al, 2 cases ofleft mandibular pain were presenred,''- Bothpatients were finally diagnosed as suffering fromischémie cardiopathy, which was referring pain tothe face.

Headache and ear pain can also be cotrelatedwith coronary disease and should be included inthe differential diagnosis, Takayanagi et al"*̂reported 2 fatal cases of angina pectoris in patientswho complained primarily of headache. Grace etal'^ reported a case of angma manifesting as vertexand occipital headache provoked by exercise andrelieved by rest. After bypass surgery rhe patientbecame pain-free. Ishida et al"""* reported a 64-year-old male who complained of headache, withoutchest pain, at the onset of a myocardial infarction.The authors concluded that the headache was dueto referred pain rather than a generalizedvasospastic disorder. At this time, the underlyingmechanisms of headache related to myocardialischemia are still not clear. Rothwcll''^ reporred 2cases in which cardiac ischemia presenred withpain confined to the ear. In both cases the diagno-sis was missed and the treatment delaved.

Case Report

A 63-year-old man reported to the dental officewith a complaint of moderate to severe pain in theleft mandibular molar and premolar dentoalveolararea. The pain was episodic anci had a consistentduration of 1 to 2 hours. The pain occurred everyday in rhe evening and tended ro decrease in inten-sity when the patient went to sleep. There was nopain upon awakening, and the patient remainedpain-free until the next evening. In the same loca-tion as the pain was a periodontally compromisedfixed partial denture with mobility. The local den-tal conditions made the diagnosis more difficult,since a local source of pain was certainly possible(Fig 2). Although dental pain was the chief com-plaint, upon questioning, the patient revealed arecent history of thoracic pain that irradiated tothe left arm. The patient was immediately referredto a cardiologist, who performed an EKG. Theresult of this test was normal. Since the clinicalcharacteristics of the pain were atypical for dentalor periodontal sources and the recent history of

Fig 2 Periapical radiograph ul ilic rcgutii reported bythe patient as painful. The periodontal conditiun and can-tilever fixed partial denture add suspicion to a possibledental diagnosis. The history and clinical characteristicsof the pain, however, did tiot confirm a dental etiology.

possihle angina pectoris had been reported, nodental therapy was performed immediately.Instead, the patient was asked to report to theemergency unit of rhe hospital the next rime he feltany chest, mandible, or tooth pain. During thenext pain episode, cardiologie examinationrevealed EKG abnormalities. Subsequently, angio-graphie studies were performed and revealed coro-nary occlusion. An angioplastic procedure wasperformed, which resolved both the coronaryocclusion and the tooth pain (Fig 3),

Conclusions

The mechanisms underlying referred pain arisingfrom rhe cardiac muscle are still not well under-stood. On occasion, ischémie heart disease can befelt primarily as an orofacial pain complaint.When this occurs, ir poses a diagnostic challengefor the clinician. An understanding of the patho-logic mechanisms and clinical features of cardiacpain and referred pain is essential for a correctdiagnosis. An improper diagnosis can lead tounnecessary dental treatment or, even more signifi-cant, a delay of proper treatment that may lead toan acute myocardial infarction. The clinician mustbe able to differentiate rhe site of pain from thesource of pain so that treatment will be properlydirected roward the source of pain."''

Angina pectoris typically presents as substernalpain radiating to the left arm, shoulder, and/orneck. When this occurs, a differential diagnosis is

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Figs 5a and 3b Photograph!, that reveal rhe patient's coronary irteries as depicted inangiggrams. [Left} Angiogram before the angioplasty. Note the marked constrictionof the coronary vessel before the procedure {arrow). (Right) Angiogram after theangioplasty. Note the return of the vessel to its normal size {arrows).

not extremely difficult. However, occasionally, apattent wtth angtna may present with orofacialpain as the matn complatnt.'•''•'"•''•'•''*' In such cases,a thorough htstory is the major clue in establishingthe proper dtagnosis. The quality of pain and itslocatton, duration, intensity, and precipitating aridameliorating factors are the main clues that willlead to the correcr diagnosis. A complete review ofsystems is also helpful.

When toothache is the primary pain complaint,local anesthesia of the tooth is often a helpful diag-nostic aid. When profoutid anesthesia of the toothis achieved without a reduction in pain, pain refer-ral should be suspected. One possible source of thisreferral is the cardiac muscle. Tn a potential cardiacpatient, local anesthetic without a vasoconstrictorshould be used. Often the diagnosis can be con-firmed by the development of pain concurrent withhemodynamic and electrocardiographic changes.""*Sublingual administratton of nitroglyceriti can alsobe used as a diagnostic test, but this is best done hythe cardiologist. The patient's age and sex are alsoimportant considerations, since cardiac pain ismost common in males 50 to 70 years old. Theseconditions, however, can occur in youngerpatients.**'' When the clinician suspects that atoothache is of cardiac origin, the patient should beimmediately referred for appropriate medical care.

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