Interappointment Pain Siqueira Et Al EndodTopics 2004

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  Interappointment pain:mechanisms, diagnosis, andtreatment  J. F. SIQUEIRA JR & F. BARNETT Knowledge on the causes of and the mechanisms behind interappointment pain in endodontics is of utmostimportance for the clinician to properly prevent or manage this undesirable condition. The causative factors of interappointment pain encompass mechanical, chemical, and/or microbial injury to the pulp or periradiculartissues,whichareinducedorexacerbatedduringrootcanaltreatment.Microorganismscanparticipateincausationofinterappointmentpaininthefollowingsituations:apicalextrusionofdebris;incompleteinstrumentationleadingto changes in the endodontic microbiota or in environmental conditions; and secondary intraradicular infections.Interappointment pain is almost exclusively due to the development of acute inflammation at the periradiculartissues in response to an increase in the intensity of injury coming from the root canal system. When aninterappointmentemergencyoccurs,properdiagnosisandactivetreatmentarerequiredfor thecliniciantosucceedin solving the problem. This review focuses on the mechanisms of interappointment pain, with special emphasisplaced on the causative agents and the host response to injury that can precipitate pain. In addition, diagnosticmeasures and treatment approaches to manage interappointment pain are also discussed.The occurrence of postoperative pain of mild intensity isnotarareeventevenwhenendodontictreatmenthasfollowed acceptable standards. For the most part, mildpainafterchemomechanicalpreparationcandevelopinabout10–30%ofthecases(1–3),andinmostinstancesthe patient can bear the discomfort or can make use of common analgesics, which are usually effective inrelieving symptoms. On the other hand, the develop-ment of interappointment pain of moderate to severeintensity, accompanied or not by swelling, has beendemonstrated to be an unusual occurrence. However,thesecasesusuallyconstituteatrueemergencyandvery often require unscheduled visit for treatment.Studies have reported frequencies of interappoint-ment emergencies ranging from 1.4% to 16% (3–9).Certain factors have been suggested to significantly influence the development of interappointment pain,including age, gender, tooth type, pulpal status,presence of preoperative pain, allergies, and presenceof sinus tract (3–5, 8, 9). In addition, fear of dentaltreatment, anxiety, apprehension, and possibly otherpsychological factors are known to influence thepatient’s pain perception and reaction thresholds(10). An association has been demonstrated betweenthe presence of apprehension before endodontictreatment and postoperative pain (4, 11).Knowledge on the causes of and the mechanismsbehind interappointment pain is of utmost importancefor the practitioner to properly prevent or manage thisundesirable condition. When an interappointmentemergency occurs, proper diagnosis and active treat-mentarerequiredfor thecliniciantosucceedinsolvingthe problem. This review willfocus onthe mechanismsof interappointment pain, with special emphasis placedon the causative agents and the host response to injury that can precipitate pain. Moreover, diagnostic mea-sures and treatment approaches to manage interap-pointment pain will also be discussed. 93  Endodontic Topics 2004, 7  ,  93–109 Printed in Denmark. All rights reserved  Copyright  r Blackwell Munksgaard  ENDODONTIC TOPICS 2004  Causes of interappointment pain The causative factors of interappointment pain com-prise mechanical, chemical, and/or microbial injury tothe pulp or periradicular tissues, which are induced orexacerbatedduringrootcanaltreatment(5,10).Regard-less of the type of injury, the intensity of the infla-mmatory response is directly proportional to theintensity of tissue injury (12). Because vascular eventsassociatedwithacuteinflammationusuallyresultinpain,itisconceivabletoassumethatthegreatertheintensityof the inflammatory reaction the greater the intensity of pain,eventhoughother factorscaninfluencethelatter.Mechanical and chemical injuries are often associated with iatrogenic factors, but microbial injury is arguably themajorandthemostcommoncauseofinterappoint-mentpain(10,13).Thiscanbeattestedbythefactthatthe frequency of interappointment pain has beenreported to be significantly higher in teeth with peri-radicular lesions as compared to teeth with vital pulpsand normal periradicular tissues (8, 14). Microbialinsult can also be coupled with iatrogenic factors tocause interappointment pain. Nevertheless, microbialinvolvementcanplayaroleinpaincausationevenwhenroot canal procedures have been performed judiciously and carefully. Microbial causes There are some special circumstances in which micro-organisms can cause interappointment pain. Whateverthe circumstances, interappointment pain will be mostoften a result of imbalance in host-bacteria relationshipinducedbyintracanalprocedures.Developmentofpainprecipitated by infectious agents can be dependent onseveral factors, most of which are likely to beinterconnected (15). These factors are as follows: Presence of pathogenic bacteria  The progression of periradicular diseases from asymp-tomatic to symptomatic status has not been welldocumented. As a consequence, there is no evidenceon the qualitative or quantitative shift in the endodon-tic microbiota that can accompany or cause exacerba-tions. This can make difficult the recognition of thebacterial species involved in the pathogenesis of symptomatic infections. However, circumstantial evi-dencehassuggestedthatcertainbacterialspeciescanbeassociated with symptomatic periradicular lesions.These include  Porphyromonas endodontalis, Porphyro- monas gingivalis, Prevotella   species,  Treponema denti- cola, Tannerella forsythia   (formerly   Bacteroides  forsythus  ) , Filifactor alocis, Dialister pneumosintes,Peptostreptococcus micros  , and  Finegoldia   (formerly  Peptostreptococcus  )  magna   (16–29). There is as yet apaucity of studies investigating the microbiota asso-ciated with interappointment pain. A recent study revealed that  F. nucleatum, Prevotella   species and Porphyromonas   species were frequently isolated fromflare-up cases (30). The possibility exists that thebacterial species associated with flare-ups are the sameas those involved with primarily infected root canalsassociated with symptomatic periradicular lesions,although it remains to be confirmed. A puzzling factorrelated to this issue is that several studies have alsofound those bacterial species in asymptomatic cases(18–23, 25, 31), which raises the suspicion that theiroccurrence in such cases can predispose to flare-ups,provided that bacteria are somehow favored by condi-tions brought about during endodontic intervention.Furthermore,factorsother thanthepresenceofagivenpathogenic species may certainly influence the devel-opment of periradicular pain and should also be takeninto consideration (15). Presence of virulent clonal types  Clonal types of a given pathogenic bacterial species cansignificantly diverge in their virulence ability (32–35). Adiseaseascribedtoagivenpathogenicspeciesisinfactcaused by specific virulent clonal types of that species.Thus, presence of virulent clones of candidate endo-dontic pathogens in the root canal may be a predis-posing factor for interappointment pain, provided thatconditions are created for them to exert pathogenicity. Microbial synergism or additism  Most of the presumed endodontic pathogens only showvirulenceoraremorevirulentwheninassociation with other species (36–40). This is because of synergicor additive microbial interactions, which can certainly influence virulence and play a role in symptomcausation. Number of microbial cells  The microbial load is well recognized as an importantfactor for a microorganism to cause disease. If the host Siqueira & Barnett  94   isfacedwithahighernumberofmicrobialcellsthanitisused to dealing with, acute exacerbation of theperiradicular lesion can occur. This can be accidentally precipitated by endodontic procedures (not necessarily iatrogenic ones) and causes for this will be discussedahead in this paper. Environmental cues   A virulent clone of a given pathogenic species does notalways express its virulence factors throughout itslifetime. A great deal of evidence indicates that theenvironment exerts an important role in inducing theturning on or the turning off of microbial virulencegenes (33, 41–45). Studies have demonstrated thatenvironmental changes can influence the behavior of some putative oral (and endodontic) pathogens, in-cluding  P. gingivalis, F. nucleatum, P. intermedia,  andoral treponemes (46, 47). If the root canal environ-mental conditions are in someway altered by intracanalprocedures and as a result become conducive to theexpression of virulence genes, microbial virulence canbe enhanced and interappointment pain can ensue. Host resistance  The host resistance to infection is a factor of unques-tionable importance dictating whether a disease willdevelop or not. It is well known that different indi- viduals present different patterns of resistance to infec-tions, and such differences can certainly becomeevident during individual’s lifetime (15,48). Hypothe-tically,individualswhohadreducedabilitytocopewithinfectionsmay be more proneto develop clinicalsymp-tomsafterendodonticproceduresininfectedrootcanals. Herpesvirus infection  This is a factor that can be coupled with diminishedhost resistance. Herpesviruses have the ability tointerfere with the host immune response, which may trigger overgrowth of pathogenic bacteria and/ordiminish the host resistance to infection (49, 50).Moreover, herpesviruses may induce the release of proinflammatorycytokinesbyhostdefensecells(51).A recent study observed that active infections of perira-dicular lesions by human cytomegalovirus and/orEpstein–Barr virus were significantly associated withsymptomatology (52). Thus, the possibility exists thatactive herpesvirus infections in periradicular lesionsmay initiate or contribute to flare-ups (53). Themechanisms behind herpesviruses involvement withsymptomatic periradicular lesions remain elusive.There are some situations during the endodontictreatment that can facilitate microorganisms to causeinterappointment pain. These include: (a) apical extru-sion of debris; (b) incomplete instrumentation leadingto changes in the endodontic microbiota or inenvironmental conditions; and (c) secondary intrar-adicular infections (54). (a) Apical extrusion of debris  Extrusion of infected debris to the periradicular tissuesduring chemomechanical preparation is allegedly oneof the principal causes of postoperative pain (10, 54,55). In asymptomatic periradicular lesions associated with infected teeth, there is a balance betweenmicrobial aggression from the infecting endodonticmicrobiota and the host defenses at the periradiculartissues. If during chemomechanical preparation micro-organisms are extruded into the periradicular tissues,the host will face a situation in which it is now challenged by a larger number of irritants than it wasbefore. Consequently, there will be a transient disrup-tion in the balance between aggression and defense, insuch a way that an acute inflammatory response ismounted to re-establish equilibrium.The risks of interappointment pain during thetreatment of infected cases can be even higher in theevent of overinstrumentation. In those cases, exacer-bations caused by iatrogenic overinstrumentation arelikely to develop as a result of mechanical injury to theperiradicular tissues, which is usually coupled withapical extrusion of a significant amount of debriscontaining microorganisms.The incidence of postoperative pain in re-treatmentcases with periradicular lesions has been demonstratedto be significantly high (5, 9, 56). During removal of the root filling material and further instrumentation,filling remnants and infected debris tend to be pushedaheadofthefilesandtobeforcedintotheperiradiculartissues,exacerbatinginflammation andcausing pain(9,56). Solvents used during filling removal are alsocytotoxic and may contribute to exacerbation of theperiradicular inflammation (57).Forcing microorganisms and their products into theperiradicular tissues can generate an acute inflamma- Interappointment pain  95   tory response, whose intensity will depend on thenumber and/or virulence ofthe extruded microorgan-isms.Therefore,quantitativeandqualitativefactorswillbe decisive in causation of interappointment pain as aresult of apical extrusion of debris. The quantitativefactor comprises the number of microbial cells ex-truded (microbial load), while the qualitative factorencompasses the virulence of the extruded micro-organisms. Admittedly, virtually all instrumentationtechniquespromoteapicalextrusionofdebris(58–60).However, techniques significantly diverge as to theamount of extruded debris, with some techniquesextruding less than others. Such differences in theamount of extruded debris may be crucial for thedevelopment of postoperative pain, as techniques thatextrude more debris allegedly increase the risk forexacerbation to occur. Crown-down techniques, irre-spective of whether hand or engine-driven instrumentsare used, usually extrude less debris and should beelected for the instrumentation of infected rootcanals. Therefore, the quantitative factor is more likely to be under control of the practitioner. On the otherhand, the qualitative factor is more difficult to becontrolled. If virulent clonal types of pathogenicbacterial species are present in the root canal systemand are propelled to the periradicular tissues duringinstrumentation, even a small amount of infecteddebris will have the potential to cause or exacerbateperiradicular inflammation. (b) Incomplete instrumentation  The microbiota associated with primary endodonticinfections is usually established as a mixed consortium,andalterationofpartofthisconsortiumwillaffectboththe environment and the remaining species. Potentexogenous forces represented by chemomechanicalpreparation using antimicrobial irrigants and intracanalmedication are needed to eradicate microbial commu-nitiesfromtherootcanalsystem.However,incompletechemomechanical preparation can disrupt the balance within the microbial community by eliminating someinhibitory species and leaving behind other previously inhibited species, which can then overgrow (61). If overgrown strains are virulent and/or reach sufficientnumbers, damage to the periradicular tissues can beintensified and then result in lesion exacerbation.Furthermore, environmental changes induced by incomplete instrumentation have the potential toinduce virulence genes to be turned on. As a result of the increase in microbial virulence, a previously asymptomatic case may become symptomatic. Another form of environmental change induced by endodontic intervention refers to the entrance of oxygen in the root canal. It has been suggested thatthis can alter the oxidation–reduction potential (Eh) inthe root canal and, as a consequence, acute exacerba-tioncanoccur(62).Thistheoryisbasedonthefactthatthe increase in Eh would induce microbial growthpattern to change from anaerobic to aerobic, withconsequent overgrowth of facultative bacteria. Over-growing facultative bacteria might precipitate acuteperiradicular inflammation. Proof of this theory islacking and theproponent study isfraught with seriousexperimental flaws and questionable procedures –impropersamplingprocedures,initial office incubationbefore transfer to the laboratory, tooth left open fordrainage, and incomplete instrumentation at the initialappointment (54). Because of this, this theory isconsidered only as speculative and there is no scientificevidence indicating it is valid. (c) Secondary intraradicular infections  Secondary intraradicular infections are caused by microorganisms that were not present in the primary infection and have gained entry into the root canalsystem during treatment, between appointments, oreven after the conclusion of the endodontic treatment(15). Introduction of new microorganisms into theroot canal system can occur due to several ways, themost common being a breach of the aseptic chainduring treatment (63). If the microorganisms that gainaccess to the root canal are successful in surviving intoand colonizing such a new environment, a secondary infection will establish itself and may be one of thecauses of postoperative pain, providing that the newly established microbial species are virulent and reachsufficient numbers to induce acute periradicular in-flammation. Non-microbial causes Microorganisms are deemed to be essential for induc-tion and perpetuation of periradicular diseases, in-asmuch as they usually represent a persistent source of irritation. Non-microbial factors can also induceperiradicular inflammation, which is however not Siqueira & Barnett  96 
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