1 Root Canal Infection and EndodonticApical Disease

Nestor CohencaDepartment of Endodontics and Pediatric Dentistry, University of Washington, Seattle,WA, USA

Ana Maria González AmaroDepartment of Microbiology, University Autonomous of San Luis Potosí, San LuisPotosí, Mexico

Infection control: why now?

The outcome of endodontic treatment dependson the microbiological status of the root canal. Ininflamed vital pulps, the infection is commonlylimited to the site of exposure causing a localizedinflammatory response (1, 2). However, whenaseptic technique is used, the effect of endodontictherapy is predictably high as demonstrated byseveral studies (3–7).

In infected necrotic pulps, microorganisms arepresent within the root canal system and denti-nal tubules, causing a apical inflammatory lesioncalled apical periodontitis. In these cases, endodontictreatment should be essentially directed towardthe prevention and control of pulpal and apicalinfections, as stated by Kakehashi, Stanley, andFitzgerald nearly 50 years ago (8). Unfortunately,the success of the therapy for these cases is 10–15%

Disinfection of Root Canal Systems: The Treatment of Apical Periodontitis, First Edition. Edited by Nestor Cohenca.© 2014 John Wiley & Sons, Inc. Published 2014 by John Wiley & Sons, Inc.

lower when compared to non-contaminated teeth(Table 1.1) (3–7, 9–11). What is more concerning isthe fact that this lower outcome has not changedor improved despite all the technological advance-ments the world of endodontics has seen (12). Howcome that despite the “art and science” of currentendodontic therapy, outcome studies have failedto demonstrate an increase in endodontic success?Why do we fail to predictably control the infectionafter so many years of research, experiment, andtreatment? The answer might be related to the factthat very few advances have ever targeted the realproblem, which continues to be microorganisms,especially in the apical third. The success of theendodontic treatment is possible only with anunderstanding of the molecular biology of thepathogens, their structures, synergies, and weak-nesses. No file will ever disinfect a root canal, nor isit designed for that purpose. Recognizing that our

3

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4 Background

Table 1.1 Outcome of endodontic therapy based on the presence or absence of apical periodontitis.

Author and year Cases/cohort RecallWithout apicalperiodontitis (%)

With apicalperiodontitis (%)

Strindberg (1956) 258 6 months to 10 years 93 80

Kerekes and Tronstad (1979) 491 Norway, Dental school 3–5 years 92 89

Sjogren et al. (1990) 96 Sweden, Dental school 8–10 years (91%) 96 86

Friedman et al. (2003) 92 4–6 years (20%) 92 74

Farzaneh et al. (2004) 94 Toronto, Grad students 4–6 years (48%) 94 81

Orstravik et al. (2004) Norway, Dental school 0.5–4 years (83%) 94 79

Ng et al. (2011) 702 London Grad students 4 years (83%) 83

Ricucci et al. (2011) 816 Italy (Ricucci) 5 years (87%) 92.3 82.7

endodontic therapy will end in failure if we do notfind a method to completely destroy the microbeswithin the root canal system, infection controlmust be our main goal and concern. Therefore, weshould focus our research and development onefficient and predictable methods to control theinfection and improve the endodontic treatmentand healing of apical periodontitis.

Terminology and apical definitions

The term apical periodontitis has gained increasingsupport and is used widely in current literature.The American Association of Endodontists recentlypublished the revised Glossary of EndodonticTerms (13). Some of the terms defined in theglossary are as follows:

Normal apical tissues Teeth with normal apical tis-sues that are not sensitive to percussion or pal-pation testing. The lamina dura surrounding theroot is intact and the periodontal ligament spaceis uniform.

Symptomatic apical periodontitis Inflammation, usu-ally of the apical periodontium, producingclinical symptoms including painful response tobiting and/or percussion or palpation. It may ormay not be associated with an apical radiolucentarea.

Asymptomatic apical periodontitis Inflammation anddestruction of apical periodontium that is ofpulpal origin, appears as an apical radiolucentarea and does not produce clinical symptoms.

Acute apical abscess An inflammatory reaction topulpal infection and necrosis characterized byrapid onset, spontaneous pain, tenderness of thetooth to pressure, pus formation, and swelling ofassociated tissues.

Chronic apical abscess An inflammatory reactionto pulpal infection and necrosis characterizedby gradual onset, little or no discomfort, andthe intermittent discharge of pus through anassociated sinus tract.

In biological terms, apical periodontitis means“inflammation of the periodontium.” This is abroad term to describe an inflammatory reactionin the tissues, including lateral and furcal locationsof inflammation; it does not distinguish etymolog-ically pulp-induced periodontitis from marginallyderived periodontitis. More specific pathologiessuch as granulomas and cysts were excludedbecause they do not represent a “clinical or radio-graphic” diagnostic reality, but rather a diagnosisbased on histological findings. The prevalence ofapical periodontitis has increased throughout theyears (14, 15), even in the low caries-rate adultDanish population (16).

The evolution of endodonticmicrobiology

Miller, in 1890 (17), was the first to demonstratethe presence of bacteria in necrotic human pulptissue. However, the cause and effect relationship

Root Canal Infection and Endodontic Apical Disease 5

is attributed to Kakehashi et al. (8) who experi-mented with gnotobiotic (germ-free) and normalrats. Bacterial contamination in the orally exposedpulp tissue caused necrosis and apical pathosesin normal rats. The study is considered a classicreference as it initiated a new and bright era inendodontic microbiology.

In 1966, Moller (18) established the importanceof adequate isolation for microbiological samplingand various culture media for the recovery andidentification of anaerobic microorganisms, pro-viding more relevant information regarding thetype of bacteria present in root canal systems.Bergenholtz then demonstrated the presence ofbacteria in the traumatized teeth. Despite the factthat pulp chambers were not exposed, bacterialgrowth was observed in 64% of all samples. Theflora was dominated by anaerobic microorganismsincluding Bacteroides, Corynebacterium, Peptostrep-tococcus, and Fusobacterium (19). Two years later,Sundqvist (20) demonstrated the prevalence ofanaerobic bacteria in root canals, supporting theresults obtained by Bergenholtz.

In the 1980s, the studies were more focused onunderstanding the colonization and interactionswithin the endodontic microflora. Moller investi-gated the relationship between uncontaminatednecrotic pulp and apical tissues. The study main-tained uncontaminated necrotic pulp in the rootcanal during a period of at least 6 months, andevaluated changes in the microbial flora enclosedin the root canal and its capacity to induce api-cal periodontitis (21). Using 9 monkeys (Macacafascicularis), the pulp of 78 teeth was asepti-cally necrotized. Twenty-six of the pulp chamberswere sealed and the pulp chamber remained free.Fifty-two teeth were infected with the indigenousflora. Clinical, radiographic and microbiologicaldata was recorded before and after the completionof the study. The root canals were initially unin-fected sterile in the final samples. No inflammatoryreactions were found on the 26 control teeth. On theexperimental teeth inflammatory reactions wereobserved clinically (12/52 teeth) and radiographi-cally (47/52 teeth). An average of 8 to 15 bacterialstrains were identified as facultative anaerobicbacteria including enterococci, coliforms, andanaerobic bacteria such as Bacteroides, Eubacterium,Propionibacterium, and Peptococcus, Peptostreptococ-cus. Some anaerobic bacteria not present on the

initial microbiological test were isolated on thefinal samples. Histological examination of the api-cal tissue confirmed the presence an inflammatoryreaction to the bacterial contamination (21).

In 1982, Fabricius et al. investigated the pulpsof 24 root canals, 8 in each of the 3 monkeys thatwere experimented on. Teeth were mechanicallydevitalized and exposed to the oral flora for about1 week and thereafter sealed. Microbiologic sam-pling and analysis was performed in 16 teeth (of 2of the monkeys) after 7 days of closure (initial sam-ples). Afterward, inoculation pulps were sealed fora period of 6 months. Final sampling was takenfrom the main root canal, the dentin, and the apicalregion at the same sampling session. All microbio-logic analyses were carried out quantitatively. Finalroot canal samples from the apical region showeda predominance of obligate anaerobic nonsporu-lating bacteria; in fact 85–98% of the bacterial cellswere anaerobic. The most frequently found specieswere Bacteroides and Gram-positive anaerobicrods. A lower proportion of facultative anaerobicbacteria were found; this was most pronouncedfor coliform rods in comparison with the strains ofBacteroides melaninogenicus.

Today, electron microscopy has become a greattechnology in many areas of science. Nair (22)studied the structure of the endodontic flora, itsrelationship to the dentinal wall, microbial inter-actions, and dynamics of apical inflammatoryresponse. The study was performed on humanteeth with granulomas and cysts. The resultsshowed the presence of microorganisms in all thesamples. The flora consisted of cocci, bacilli, andspirochetes filamentous organisms. In most cases,the bacteria were restricted to the canal, but in 4granulomas and 1 cyst, the bacteria were foundin the lesion. There was a distinct bacterial plaqueadhering to the dentinal wall at the apical foramen.Nair describes this finding as a group or commu-nity of one or more types of microorganisms as wellas bacterial condensate, suggesting the formationof plaque in the dentinal wall by the flora of theroot canal. This finding is considered to be thesubject that currently occupies many researchers:the presence of biofilm on root canal walls.

In 1990, Nair (23) analyzed nine therapy-resistantand asymptomatic human apical lesions (4–10years) removed during surgery using light andelectron microscopy. Six out of nine lesions revealed

6 Background

microorganisms in the apical root canal. Four con-tained bacteria and two contained yeasts. Of thethree cases with no microorganisms, one revealed aforeign body giant cell granuloma. In the majorityof therapy-resistant apical lesions, microorgan-isms (bacteria, yeast) and foreign body giant cellgranulomas play a significant role in treatmentfailures.

Although endodontic microbiology has evolvedsignificantly, it still lacks an understanding of theecology of the root canal and requires an analysisof the bond that develops between microorgan-isms and their surroundings. This relationship isan essential element that provides a glimpse intothe understanding of their behavior and ability toinvade an area that is rich in nutrients and whoseabiotic and biotic factors determine the distributionand quantity of living organisms that may sharethe root space. In the early 1990s, Sundqvist (24, 25)published a couple of reviews summarizing theavailable data. Bacterial flora of the root canal isdominated by obligate anaerobes, comprising upto 90% of the total population. Aerobic bacteria arerarely found initially in the infected root canals butcould have been introduced during the treatment.During the course of an infection, interrelation-ships develop between microbial species, based ontheir nutritional demands and nutritional interac-tions, and the pathogenicity of the polymicrobialroot flora is dependent on bacterial synergy. Bac-teriocins proteins produced by a microorganismenhance their ability to inhibit growth of somespecies competing for the same ecological niche.Additionally, they promote bacterial coaggregationand interactions establishing the ecology of theapical tissues.

The identification of the endodontic micro-biota in the apical third was reported in 1991 byBaumgartner (26) who employed both aerobicand anaerobic cultures in the same study, in orderto isolate and identify the microflora of the api-cal portion of root canals of teeth with cariouspulpal exposures and apical lesions. Ten freshlyextracted teeth with carious pulpal exposures andapical lesions contiguous with the root apex wereplaced inside an anaerobic chamber and the api-cal 5 mm of the root canals cultured. In additionto anaerobic incubation, duplicate cultures wereincubated aerobically. Fifty strains of bacteria fromthe 10 root canals were isolated and identified.

The most prominent bacteria cultured from the10 root canals were Actinomyces, Lactobacillus,black-pigmented Bacteroides, Peptostreptococcus,nonpigmented Bacteroides, Veillonella, Enterococcusfaecalis, Fusobacterium nucleatum, and Streptococcusmutans. Of the 50 bacterial isolates, 34 (68%) werestrict anaerobes. Baumgartner’s study demon-strated the presence of predominantly anaerobicbacteria in the apical 5 mm of infected root canalsin teeth with carious pulpal exposures and apicallesions.

Advancements in the identification of endodon-tic flora by Molander et al. in 1998 correlatedthe clinical outcome, refractory lesions, and thepresence of certain strains. Molander and cowork-ers examined the microbiological status of 100root-filled teeth with radiographically verifiedapical periodontitis and 20 teeth without signs ofapical pathoses. In teeth with apical periodontitis,117 strains of bacteria were recovered in 68 teeth.Facultative anaerobic species predominated amongthese isolates (69% of identified strains). Entero-cocci were the most frequently isolated genera,showing “heavy” or “very heavy” growth in 25out of 32 cases (78%). In 11 teeth without signs ofapical pathoses, no bacteria were recovered whilethe remaining 9 yielded 13 microbial strains. Eightof these grew “very sparsely.” It was concludedthat the microflora of the obturated canal differsfrom that found normally in the untreated necroticdental pulp, quantitatively as well as qualitatively.

In 1990, Sha and Collins reclassified the moder-ately saccharolytic, predominantly oral Bacteroidesspecies, which include B. melaninogenicus, Bac-teroides oralis, and related species. These bacteriaform a phenotypically and phylogenetically coher-ent group of species, which differ so significantlyfrom the emended description of the genus Bac-teroides that they should not be classified inthe same genus and proposed that these speciesbe reclassified in a new genus, Prevotella (27)(Figure 1.1).

By this time the advent of molecular biologytechniques advanced in leaps and bounds in thedetection and identification of microorganisms,uncovering the intimacy between genetics, bio-chemistry, and microbiology. Technique sensitiveanalyses of nucleic acids extracted from microor-ganisms directly, or from a sample containingthe microorganism in question, have identified

Root Canal Infection and Endodontic Apical Disease 7

New black-pigmentedclassification

Porphyromonas (Asaccharolytic)

Prevotella (Saccharolytic)

– Porphyromonas gingivalis– Porphyromonas endodontalis

– Prevotella intermedius– Prevotella melaninogenicus– Prevotella denticola– Prevotella loescheii– Prevotella nigrescens– Prevotella corporis

Figure 1.1 Current taxonomy and of black-pigmentedbacteria.

endodontic microorganisms of interest; as was thecase with Actinomyces. Polymerase chain reaction(PCR) is a biochemical technology in molecularbiology used to amplify a single or a few copies ofa piece of DNA across several orders of magnitude,generating thousands to millions of copies of aparticular DNA sequence. Xia and Baumgartnerused PCR with a pair of universal primers for Acti-nomyces and species-specific primers to evaluatethe contents of infected root canals and aspiratesfrom abscesses or cellulitis for the presence ofActinomyces israelii, Actinomyces naeslundii, andActinomyces viscosus. DNA was extracted from131 clinical samples (28). DNA reacting with theuniversal primer for Actinomyces was detectedin 72 of 129 (55.8%) clinical samples. Of those, 41of 51 (80.4%) were from infected root canals, 22 of48 (45.8%) were from abscesses, and 9 of 30 (30%)were associated with cellulitis.

Since then, Siqueira and Rocas reported hun-dreds of species obtained from root canals usingPCR techniques. In a review article published in2008, they concluded that bacterial presence in theroot canal at the time of filling is a risk factor forposttreatment apical periodontitis (29). About 100species/phylotypes have already been detectedin postinstrumentation and/or postmedicationsamples, and Gram-positive bacteria are the mostdominant. However, it remains to be determinedby longitudinal studies if any species/phylotypespersisting after treatment procedures can influencethe outcome (29).

Waltimo et al. reported the current trend ofrecurrent yeast in endodontic infections, and theirantimicrobial response confirms that yeast may beisolated in about 5–20% of the infected root canals.Their article identifies multiple virulence factors ofCandida that allow it to infect the dentin–pulp com-plex and penetrate the dentinal tubules causing aninflammatory reaction and suggesting a pathogenicrole of this organism in apical periodontitis (30).

With the discovery and understanding thatfungus is present, the complexity of the micro-biota became clear. In 2003, Slots et al. (31) werethe first to report the presence of cytomegalovirusand Epstein–Barr virus (EBV) in more than 90%of granulomas of symptomatic and large apicallesions (31). Dual infection with cytomegalovirusand EBV is closely associated with symptomaticlesions. Herpes simplex virus’ (HSV) active infectionhas no apparent relationship to apical disease.

Another study aimed to identify herpes virus,including human cytomegalovirus (HCMV), EBV,HSV-1, and varicella zoster virus (VZV) in-vivo(32, 33). Patients with acute apical abscesses andcellulitis of endodontic origin were used for thestudy. The identification was carried out by theprimary PCR and nested PCR techniques. Theresults demonstrated the presence of HCMV, EBV,and HSV-1; however, they indicated that the pres-ence of herpes virus that were identified were verylow in their genetic copies, and therefore it wasconcluded that herpes viruses are present but donot have a direct relation to the development orestablishment of pathologies such as acute apicalabscess or cellulitis of endodontic origin.

The link between endodontic infectionand apical disease

The presence of bacteria within the root canalsystem is essential for the development of apicalinflammation (8). Apical periodontitis is a diseasecharacterized by inflammation and destructionof apical tissues caused by microbial agentsof endodontic origin. Initially, the tooth pulpbecomes infected and necrotic by an autogenousoral microflora. The microenvironment of rootcanal systems provides excellent conditions forthe establishment of a mixed, predominantlyanaerobic, flora. Collectively, this polymicrobial

8 Background

community residing in the root canal has severalbiological and pathogenic properties, such as anti-genicity, mitogenic activity, chemotaxis, enzymatichistolysis, and activation of host cells.

Microorganisms’ growth within the root canalis in the form of biofilm. The microbial com-munity develops as a biofilm and colonizes theenvironment. It occurs first by the depositionof a conditioning film; then there is adhesionand colonization of planktonic microorganismsin a polymeric matrix. The coadhesion of otherorganisms and the detachment of biofilm microor-ganisms into their surroundings happen at a laterstage (34). Bacterial biofilm has an open architec-ture with channels traversing from the biofilmsurface. The structure of biofilm affects the move-ment of molecules, and the gradients are keydeterminants in its development. Bacteria growingon a surface may display a novel phenotype that,consequently, may allow increased resistance toantimicrobial agents. Resistance can result fromrestricted inhibitor penetration, slower bacterialgrowth rates, transfer of resistance genes, subopti-mal environmental conditions for inhibitor activity,and the expression of a resistant phenotype (35).

This ecological view on the persisting infectionin endodontics suggests that the action of individ-ual species in refractory endodontic infections issecondary when compared to the adaptive changesof a polymicrobial biofilm community undergoingphysiological and genetic changes in response tochanges in the root canal environment (36). Theinvasion of root dentinal tubules by root canalbacteria is a multifactorial event in which a limitednumber of oral bacterial species have the requiredproperties to participate. Current literature hasdemonstrated that biofilms may remain viablein anatomical areas of the root canal system thatremain untouched by either mechanical or chem-ical disinfection (Figure 1.2) (37–39). Scanningelectron microscopy (SEM) examination of root tipsassociated with refractory apical periodontitis hassuggested the presence of bacterial biofilm at theapical portion of the root canal (Figure 1.3) (40–42).

SEM analysis revealed bacterial biofilm sur-rounding the apical foramen and external radicularsurface (Figures 1.4a and 1.2c). Careful observationof these structures under higher magnificationrevealed clumps of coaggregated bacterial cellsin a matrix of extracellular polymeric substance

(EPS). E. faecalis biofilms displayed a complexthree-dimensional structure that demonstratedspatial heterogeneity and a typical architectureshowing microcolonies with ramifying water chan-nels (Figure 1.4b). Fibrillar structures appeared tobe made up of twisted fibers. Larger structures ofwrapped sheets were also present and consistedof small numbers of bacteria cells embedded in amatrix of fibers (Figure 1.4d).

Bacterial endotoxins and by-products egressthrough portals of exit causing the destruction ofthe apical tissues. In response, the host has an arrayof defenses consisting of several classes of cells,intercellular messengers, antibodies, and effectormolecules. The microbial factors and host defenseforces encounter, clash with, and destroy much ofthe apical tissue, which result in the formation ofvarious categories of apical periodontitis lesions.In spite of the formidable defense, the body isunable to destroy the microbes well-entrenchedin the sanctuary of the necrotic root canal, whichis beyond the body’s immune system. Therefore,the major goal of the root canal debridement is toeliminate the biofilm and bacteria-harboring debris.

Contemporary endodontic microbiology hasbecome even more complex with the discoveryof fungi and viruses. Waltimo et al. (43) foundyeast in 7% of the culture-positive samples frompersistent root canal infections. Candida albicanswas the most frequently isolated yeast (80%). Thisfinding was later confirmed by several studies (44,45). Attachment to mucosal tissues and to abioticsurfaces and the formation of biofilms are crucialsteps for Candida survival and proliferation in theoral cavity. Candida species possess a wide arsenalof glycoproteins located at the exterior side ofthe cell wall, many of which play a determiningrole in these steps. In addition, C. albicans secretessignaling molecules that inhibit the yeast-to-hyphatransition and biofilm formation. In-vivo, Candidaspecies are members of mixed biofilms and subjectto various antagonistic and synergistic interactions(Figure 1.5) (46). Recently, Gomes et al. (47) con-firmed the presence of filamentous fungi, whichwere isolated in situ from 17 of 60 samples (28.3%).The genus Aspergillus was isolated from 7/17samples (41%).

The presence of HCMV, EBV, and HSV was firstreported by Sabeti et al. (48) in symptomatic apicallesions. In a different study, Slots et al. (49) detected

Root Canal Infection and Endodontic Apical Disease 9

(a)

(d)

(b)

(c) (f)

(e)

Figure 1.2 Composite figure ofphotomicrographs representative ofmicroscopic sections of Groups I(EndoVac—ANP), II (Ultrasound—PUI),and III (conventional irrigation—PP)stained by the Brown and Brenntechnique, revealing the presence andlocation of bacteria in the root canalsystem and apical tissues 180 days afterendodontic treatment: (a) Panoramicphotomicrograph, showingcontamination of the entire extension ofthe tooth (Zeiss, 1.25×). (b) Detail ofpanel a (rectangle) in which the cervicalroot canal third can be visualized withabundant presence of microorganismsinside the dentinal tubules (Zeiss, 20×).(c) Detail of panel a (square) showingthe middle root canal third with intensepresence of bacteria (Zeiss, 20×). (d)Detail of panel a (circle) revealing themiddle root canal third with presence ofbacteria in the cemental craters (arrow)(Zeiss, 10×). (e) Detail of panel a(triangle) showing abundant presence ofmicroorganisms in the apical root canalthird (Zeiss, 40×). (f) Detail of panel a(asterisk) in which bacteria can be seenin the apical lesion (Zeiss, 20×).

HCMV in 100% of the symptomatic and in 37%of the asymptomatic study lesions (49). EBV wasidentified only in HCMV-infected apical lesions.The difference of HCMV and EBV between symp-tomatic and asymptomatic lesions was found to bestatistically significant. Current studies confirmedthese findings by using primary and nested PCR aswell as reverse transcription PCR. (33) EBV DNAand RNA were present in endodontic pathoses insignificantly higher percentages (43.9% and 25.6%,respectively) compared with healthy pulp controls.

The DNA of HSV was found in low percentages inendodontic patients (13.4%), and only one patientshowed the presence of VZV. In conclusion, thepresence of fungi and viruses had been associatedwith irreversible pulpitis and periodontitis, con-firming once again that endodontic micro flora iscomplex and composed of well-organized biofilmsof microorganisms with synergetic interactions.

The host responses to root canal infection havebeen the subject of much research in recent years.There is great similarity among the pathogenic

10 Background

(a) (b)

(d)(c)

Figure 1.3 In-vivo E. faecalis biofilm. (a, c) Cocoidal structures attached to mature biofilm (6000×). (b) Extrapolymeric fibers(10,000×). (d) “Mushroom”-shaped structures (10,000×).

(a) (b)

(c) (d)

Figure 1.4 E. faecalis mature biofilm in-vivo. (a, c) Microcolonies wrapped in an extracellular matrix (8000×). (b) Networkconsisting of fibrillary structures (10,000×). (d) “Mushroom”-shaped structures (10,000×).

Root Canal Infection and Endodontic Apical Disease 11

Figure 1.5 Mature biofilm demonstrating the synergistic relationship between E. faecalis and Candida albicans.

processes in marginal and apical periodontitis, andmany of the findings in periodontal research havedirect relevance to apical periodontitis. A clearerconcept of the immunological processes involved inthe development of apical periodontitis is emerging(50, 51). Microbiological variability and virulencefactors in infected root canals have been demon-strated, and specific data indicate that the bacterialflora varies systematically with the clinical con-dition of the tooth involved (persistent infection,therapy-resistant infection). Different therapeu-tic strategies of antimicrobial control may haveto be applied, depending on the microbiologicaldiagnosis in a given case.

Apical periodontitis is not a self-healing disease(52). Untreated apical periodontitis may lead toa chronic infection of the oral tissues at locationscloser to more vital organs than many other oralinfections. Although these infections may remainquiescent for decades, they may also develop andspread with serious consequences for the individ-ual (53, 54). In the face of the risks of such chronicinfection from the infected teeth, their extraction

and replacement by implants has been put forwardand discussed as a viable alternative to endodon-tic treatment (55, 56). The variable success rates(by strict criteria) of treatment procedures for thecure of apical periodontitis are sometimes used asarguments for the implant “treatment” concept.However, what little evidence there is does notindicate a lower survival rate of endodonticallytreated teeth, and the superiority of tooth preser-vation compared to its replacement should beevident as a biological principle of preference.However, the challenge from other treatment con-cepts, to endodontics as a discipline, should act asa driving force to produce more and scientificallysolid evidence for the modalities of cure and pre-vention applied to our disease of interest, apicalperiodontitis.

Conclusion

Pulpal and apical inflammation, and the asso-ciated pain and the consequences of root canal

12 Background

infection, remain significant aspects of dentistrytoday. New knowledge and insights provide bet-ter treatment opportunities and stimulate furtherresearch activities. The prevention and control ofapical periodontitis has a solid scientific base butthe many variations in the clinical manifestationsof the disease still leave technical and biologicalproblems that need to be solved. Despite recenttechnological advances in treatment, evidence ofimproved outcome is still lacking. Alternativetreatment involving implants is promoted as beingbetter, but the criteria of evaluation of the outcomeof the two forms of treatment are dissimilar; there isno true evidence-based comparison. The advance-ment, and utilization, of our biologic principleswill allow a better understanding of the diseaseprocess and add to the fundamental truth thatthe biologic response to disease continues to bea biologic therapy; those therapies will and mustcontinue to advance with our understanding.

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Root Canal Infection and Endodontic Apical Disease 13

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