On the causes of persistent apical periodontitis

33 Pages·2006·4.29 MB·English

REVIEW
On the causes of persistent apical periodontitis:
a review
P. N. R. Nair
InstituteofOralBiology,SectionofOralStructuresandDevelopment,CentreofDentalandOralMedicine,UniversityofZurich,
Zurich,Switzerland
Abstract apicalperiodontitispersistingafterrootcanaltreatment
havenotbeenwellcharacterized.Duringthe1990s,a
Nair PNR. Onthecausesofpersistentapicalperiodontitis:a
series of investigations have shown that there are six
review.InternationalEndodonticJournal,39,249–281,2006.
biological factors that lead to asymptomatic radiolu-
Apicalperiodontitisisachronicinflammatorydisorder cenciespersistingafterrootcanaltreatment.Theseare:
ofperiradiculartissuescausedbyaetiologicalagentsof (i) intraradicular infection persisting in the complex
endodonticorigin.Persistentapicalperiodontitisoccurs apical root canal system; (ii) extraradicular infection,
when root canal treatment of apical periodontitis has generally in the form of periapical actinomycosis; (iii)
not adequately eliminated intraradicular infection. extrudedrootcanalfillingorotherexogenousmaterials
Problems that lead to persistent apical periodontitis thatcauseaforeignbodyreaction;(iv)accumulationof
include: inadequate aseptic control, poor access cavity endogenous cholesterol crystals that irritate periapical
design, missed canals, inadequate instrumentation, tissues; (v) true cystic lesions, and (vi) scar tissue
debridement and leaking temporary or permanent healing of the lesion. This article provides a compre-
restorations.Evenwhenthemoststringentprocedures hensive overview of the causative factors of
are followed, apical periodontitis may still persist as non-resolving periapical lesions that are seen as
asymptomatic radiolucencies, because of the complex- asymptomatic radiolucencies post-treatment.
ity of the root canal system formed by the main and
Keywords: aetiology, endodontic failures, persistent
accessory canals, their ramifications and anastomoses
apical radiolucency, non-healing apical periodontitis,
whereresidualinfectioncanpersist.Further,thereare
refractoryperiapicallesions,persistentapicalperiodon-
extraradicular factors – located within the inflamed
titis.
periapical tissue – that can interfere with post-treat-
ment healing of apical periodontitis. The causes of Received27September2005;accepted24November2005
infection within the root canal system of the affected
tooth (Kakehashi etal. 1965, Sundqvist 1976). The
Introduction
infected and necrotic pulp offers a selective habitat for
Apical periodontitis is an inflammatory disorder of the organisms (Fabricius et al. 1982b). The microbes
periradicular tissues caused by persistent microbial grow in sessile biofilms, aggregates, coaggregates, and
alsoasplanktoniccellssuspendedinthefluidphaseof
thecanal(Nair1987).Abiofilm(Costertonetal.2003)
Correspondence: Dr P. N. R. Nair, Institute of Oral Biology, is a community of microorganisms embedded in an
SectionofOralStructuresandDevelopment(OSD),Centreof
exopolysaccharide matrix that adheres onto a moist
Dental & Oral Medicine, University of Zurich, Plattenstrasse
11, CH-8028 Zurich, Switzerland (Tel.: [phone]; surfacewhereasplanktonicorganismsarefree-floating
fax:[phone];e-mail:[email protected]). single microbial cells in an aqueous environment.
ª2006InternationalEndodonticJournal InternationalEndodonticJournal,39,249–281,2006 249
Persistentapicalperiodontitis Nair
Microorganisms protected in biofilms are greater than of lesions may persist radiographically, because of the
one thousand times more resistant to biocides as the anatomical complexity of the root canal system (Hess
same organisms in planktonic form (Wilson 1996, 1921, Perrini & Castagnola 1998) with regions that
Costerton &Stewart 2000). cannot be debrided and obturated with existing
Thereisconsensusthatapicalperiodontitispersisting instruments, materials and techniques (Nair et al.
after root canal treatment presents a more complex 2005). In addition, there are factors located beyond
aetiological and therapeutic situation than apical the root canal system, within the inflamed periapical
periodontitis affecting teeth that have not undergone tissue, that can interfere with post-treatment healing
endodontic treatment. The aetiological spectrum and of the lesion (Nair & Schroeder 1984, Sjo¨gren et al.
treatment options of persistent apical periodontitis are 1988, Figdor et al. 1992, Nair et al. 1999, Nair
broader than those of teeth that have not undergone 2003a,b).
previous root canal treatment. Further, the process of
decision-making regardingthemanagementofpersist-
Microbial causes
ent apical periodontitis is more complex and less
uniform among clinicians than in the management of
Intraradicular infection
apical periodontitis affecting non-treated teeth (Fried-
man 2003). For optimum clinical management of the Microscopical examination of periapical tissues
disease a clear understanding of the aetiology and removed by surgery has long been a method to detect
pathogenesis of the disease is essential. Therefore, the potential causative agents of persistent apical perio-
purposeofthiscommunicationistoprovideacompre- dontitis. Early investigations (Seltzer et al. 1967, And-
hensive overview of the causes and maintenance of reasen&Rud1972,Blocket al.1976,Langelandet al.
persistent apical periodontitis that is radiographically 1977, Lin et al. 1991) of apical biopsies had several
visualized as periapical radiolucencies which are often limitations such as the use of unsuitable specimens,
asymptomatic. inappropriate methodology and criteria of analysis.
Intraradicular microorganisms being the essential Therefore,thesestudiesdidnotyieldrelevantinforma-
aetiological agents of apical periodontitis (Kakehashi tionaboutthereasonsforapicalperiodontitispersisting
et al. 1965, Sundqvist 1976), the treatment of the as asymptomatic radiolucencies even after proper root
disease consists of eradicating the root canal microbes canaltreatment.
or substantially reducing the microbial load and In one histological analysis (Seltzer etal. 1967) of
preventing re-infection by root canal filling (Nair et al. persistent apical periodontitis, there was not even a
2005). When the treatment is done properly, healing mentionofresidualmicrobialinfectionoftherootcanal
oftheperiapicallesionusuallyoccurswithhardtissue system as a potential cause of the lesions remaining
regeneration, that is characterized by reduction of the unhealed. A histobacteriological study (Andreasen &
radiolucency on follow-up radiographs (Strindberg Rud 1972) using step-serial sectioning and special
1956, Grahne´n & Hansson 1961, Seltzer et al. bacterial stains, found bacteria in the root canals of
1963, Storms 1969, Molven 1976, Kerekes & 14%ofthe66specimensexamined.Twootherstudies
Tronstad 1979, Molven & Halse 1988, Sjo¨gren et al. (Block et al. 1976, Langeland etal. 1977) analysed
1990, 1997, Sundqvist et al. 1998). Nevertheless, a 230and35periapicalsurgicalspecimens,respectively,
completehealingofcalcifiedtissuesorreductionofthe by routine paraffin histology. Although bacteria were
apical radiolucency does not occur in all root canal- foundin10%and15%oftherespectivebiopsies,only
treated teeth. Such cases of non-resolving periapical in a single specimen in each study was intraradicular
radiolucencies are also referred to as endodontic infection detected. In the remaining biopsies in which
failures. Periapical radiolucencies persist when treat- bacteria were found, the data also included those
ment procedures have not reached a satisfactory specimens in which bacteria were found as ‘contami-
standard for the control and elimination of infection. nantsonthesurfaceofthetissue’.Inyetanotherstudy
Inadequate aseptic control, poor access cavity design, (Lin et al. 1991) ‘bacteria and or debris’ was found in
missed canals, insufficient instrumentation, and leak- the root canals of 63% of the 86 endodontic surgical
ing temporary or permanent restorations are common specimens, although it is obvious that ‘bacteria and
problems that may lead to persistent apical periodon- debris’cannotbeequatedaspotentialcausativeagents.
titis (Sundqvist & Figdor 1998). Even when the most Thelow reportedincidenceof intraradicular infections
careful clinical procedures are followed, a proportion in these studies is primarily due to a methodological
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Nair Persistentapicalperiodontitis
inadequacy as microorganisms easily go undetected 1921, Perrini & Castagnola 1998) and the ecological
when the investigations are based on random paraffin organization of the flora into protected sessile biofilms
sectionsalone.Thishasbeenconvincinglydemonstra- (Costerton & Stewart 2000, Costerton etal. 2003)
ted (Nair 1987, Nair et al. 1990a). Consequently, composed of microbial cells embedded in a hydrated
historic studies on post-treatment apical periodontitis exopolysaccharide-complex in micro-colonies (Nair
didnotconsiderresidualintraradicularinfectionasan 1987), it is very unlikely that an absolutely microor-
aetiological causative factor. ganism-freecanal-systemcanbeachievedbyanyofthe
Inordertoidentifytheaetiologicalagentsofasymp- contemporaryrootcanalpreparation,cleaningandroot
tomaticpersistentapicalperiodontitisbymicroscopy,the fillingprocedures.Then,thequestionarisesastowhya
casesmustbeselectedfromteeththathavehadthebest large number of apical lesions heal after non-surgical
possible root canal treatment and the radiographic rootcanaltreatment.Someperiapicallesionshealeven
lesionsremainasymptomaticuntilsurgicalintervention. wheninfectionpersistsinthecanalsatthetimeofroot
The specimens must be anatomically intact block- filling (Sjo¨gren et al. 1997). Although this may imply
biopsiesthatincludetheapicalportionoftherootsand thattheorganismsmaynotsurvivepost-treatment,itis
the inflamed soft tissue of the lesions. Such specimens more likely that the microbes may be present in
should undergo meticulous investigation by serial or quantities and virulence that may be sub-critical to
step-serial sections that are analysed using correlative sustain the inflammation of the periapex (Nair et al.
lightandtransmissionelectronmicroscopy.Astudythat 2005).Insomecasessuchresidualmicrobescandelayor
metthesecriteriaandalsoincludedmicrobialmonitor- preventperiapicalhealingaswasthecasewithsixofthe
ing before and during treatment (Nair et al. 1990a) ninebiopsiesstudiedandreported(Nairet al.1990a).
revealedintraradicularmicroorganismsinsixofthenine On the basis of cell wall ultrastructure only Gram-
block biopsies (Fig.1). The finding showed that the positive bacteria were found (Nair et al. 1990a)
majorityofrootcanal-treatedteethwithasymptomatic (Fig.2), an observation fully in agreement with the
apicalperiodontitisharbouredpersistentinfectioninthe results of purely microbiological investigations of root
apical portion of the complexroot canal system. How- canals of previously root filled teeth with persisting
ever, the proportion of cases with persistent apical periapical lesions. Of the six specimens that contained
periodontitishavingintraradicularinfectionislikelyto intraradicular infections, four had one or more mor-
bemuchhigherinroutineendodonticpracticethanthe phologicallydistincttypesofbacteriaandtworevealed
two-thirdsoftheninecasesreported(Nairet al.1990a) yeasts(Fig.3).Thepresenceofintracanalfungiinroot-
forseveralreasons.Atthelightmicroscopiclevelitwas treated teeth with apical periodontitis was also con-
possible to detect bacteria in only one of the six cases firmed by microbiological techniques (Waltimo et al.
(Nair et al. 1990a). Microorganisms were found as a 1997, Peciuliene etal. 2001). These findings clearly
biofilmlocatedwithinthesmallcanalsofapicalramifi- associate intraradicular fungi as a potential non-bacter-
cations(Fig. 1)intherootcanalorinthespacebetween ial, microbial cause of persistent apical lesions. Intra-
the root fillings and canal wall. This demonstrates the radicular infection can also remain within the
inadequacyofconventionalparaffintechniquestodetect innermostportionsofinfecteddentinaltubulestoserve
infectionsinapicalbiopsies. as a reservoir for endodontic reinfection that might
The microbial status of apical root canal systems interfere with periapical healing (Shovelton 1964,
immediatelyafternon-surgicalrootcanaltreatmentwas Valderhaug 1974, Nagaoka et al. 1995, Peters et al.
unknown.However,inarecentstudy(Nairetal.2005), 1995, Loveet al. 1997, Love &Jenkinson 2002).
14 of the 16 root filled mandibular molars contained
residual infection in mesial roots when the treatment Microbial flora of rootcanal-treated teeth
was completed in one-visit and includes instrumenta- The endodontic microbiology of treated teeth is less
tion, irrigation with NaOCl and filling. The infectious understood than that of untreated infected necrotic
agents were mostly located in the uninstrumented dental pulps. This has been suggested to be a conse-
recessesofthemaincanals,isthmusescommunicating quence of searching for non-microbial causes of a
them and accessory canals. The microbes in such purelytechnicalnatureforlesionspersistent afterroot
untouched locations existed primarily as biofilms that canal treatments (Sundqvist & Figdor 1998). Only a
were not removed by instrumentation and irrigation small number of species has been found in the root
withNaOCl.Inviewofthegreatanatomicalcomplexity canalsofteeththathaveundergoneproperendodontic
of the root canal system, particularly of molars (Hess treatment that, on follow-up, revealed persisting,
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Persistentapicalperiodontitis Nair
Figure1 Light microscopic view of axial semithin sections through the surgically removed apical portion of the root with a
persistentapicalperiodontitis.Notetheadhesivebiofilm(BF)intherootcanal.Consecutivesections(a,b)revealtheemerging
widenedprofileofanaccessorycanal(AC)thatiscloggedwiththebiofilm.TheACandthebiofilmaremagnifiedin(c)and(d)
respectively.Magnifications:(a)·75,(b)·70,(c)·110,(d)·300.AdaptedfromNairetal.(1990a).
252 InternationalEndodonticJournal,39,249–281,2006 ª2006InternationalEndodonticJournal
Nair Persistentapicalperiodontitis
Figure2 Transmissionelectronmicroscopicviewofthebiofilm(BAupperinset)illustratedinFig.1.Morphologicallythebacterial
populationappearstobecomposedofonlyGram-positive,filamentousorganisms(arrowheadinlowerinset).Notethedistinctive
Gram-positivecellwall.Theupperinsetisalightmicroscopicviewofthebiofilm(BA).Magnifications:·3400;insets:upper·135,
lower·21300.FromNairetal.(1990a).PrintedwithpermissionfromLippincottWilliams&Wilkins(cid:1).
asymptomatic periapical radiolucencies. The bacteria ococcus and Propionibacterium (previously Arachnia)
found in these cases are predominantly Gram-positive are frequently isolated and characterized from such
cocci,rodsandfilaments.Byculture-basedtechniques, root canals (Mo¨ller 1966, Sundqvist & Reuterving
species belonging to the genera Actinomyces, Enter- 1980, Happonen 1986, Sjo¨gren et al. 1988,
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Persistentapicalperiodontitis Nair
Figure3 Fungiasapotentialcauseofnon-healedapicalperiodontitis.(a)Low-powerviewofanaxialsectionofaroot-filled(RF)
toothwithapersistentapicalperiodontitis(GR).Therectangulardemarcatedareasin(a)and(d)aremagnifiedin(d)and(b),
respectively.Notethetwomicrobialclusters(arrowheadsinb)furthermagnifiedin(c).Theovalinsetin(d)isatransmission
electronmicroscopicviewoftheorganisms.Notetheelectron-lucentcellwall(CW),nuclei(N)andbuddingforms(BU).Original
magnifications:(a)·35,(b)·130,(c)·330,(d)·60,ovalinset·3400.AdaptedfromNairetal.(1990a).Printedwithpermission
fromLippincottWilliams&Wilkinsª.
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Fukushima et al. 1990, Molander et al. 1998, isolatedfungusfromrootfilledteethwithapicalperio-
Sundqvist et al. 1998, Hancock et al. 2001, Pinheiro dontitis(Molanderet al.1998,Sundqvistet al.1998).
et al. 2003). The presence of Enterococcus faecalis in
cases of persistent apical periodontitis is of particular
Extraradicular infection
interest because it is rarely found in infected but
untreated root canals (Sundqvist & Figdor 1998). Actinomycosis
Enterococcus faecalis is the most consistently reported Actinomycosis is a chronic, granulomatous, infectious
organism from such former cases, with a prevalence disease in humans and animals caused by the genera
ranging from 22% to 77% of cases analysed (Mo¨ller Actinomyces and Propionibacterium (McGhee et al.
1966, Molander et al. 1998, Sundqvist et al. 1998, 1982).Theaetiologicalagentofbovineactinomycosis,
Peciuliene et al. 2000, Hancock etal. 2001, Pinheiro Actinomyces bovis, was the first species to be identified
et al.2003,Siqueira&Roˆc¸as2004,Fouadetal.2005). (Harz 1879). The disease in cattle, known as ‘lumpy
The organism is resistant to most of the intracanal jaw’or‘bigheaddisease’,ischaracterizedbyextensive
medicaments,andcantolerate(Bystro¨met al.1985)a bonerarefaction, swelling of thejaw,suppurationand
pH up to 11.5, which may be one reason why this fistulation.Thecausativeagentsweredescribedasnon-
organism survives antimicrobial treatment with cal- acid fast, non-motile, Gram-positive organisms reveal-
ciumhydroxidedressings.Thisresistanceoccursprob- ingcharacteristicbranchingfilamentsthatendinclubs
ablybyvirtueofitsabilitytoregulateinternalpHwith or hyphae. Because of the morphological appearance
an efficient proton pump (Evans et al. 2002). Entero- these organisms were considered fungi and the taxon-
coccusfaecaliscansurviveprolongedstarvation(Figdor omy of Actinomyces remained controversial for more
et al. 2003). It can grow as monoinfection in treated than a century. The intertwining filamentous colonies
canalsintheabsenceofsynergisticsupportfromother are often called ‘sulphur granules’ because of their
bacteria(Fabriciusetal.1982a).Therefore,E.faecalisis appearance as yellow specks in exudates. On careful
regarded as being a very recalcitrant microbe among crushing, the tiny clumps of branching microorgan-
the potential aetiological agents of persistent apical isms with radiating filaments in pus, give a ‘starburst
periodontitis. However, the presence of E. faecalis in appearance’ which prompted Harz (1879) to coin the
casesofpersistentapicalperiodontitisisnotauniversal name Actinomyces or ‘ray fungus’. Four years later
observation. This is because one microbial culture Actinomyces israelii was isolated from humans in pure
(Cheung & Ho 2001) and a molecular based (Rolph culture,characterizedanditspathogenicityinanimals
et al.2001)study,inwhichthepresenceofE.faecalisin demonstrated(Wolff&Israel1891).Manyresearchers,
such cases was investigated, failed to detect the nevertheless,consideredthehumanandbovineisolates
organism. Further, the prevalence of E. faecalis was as identical. However, A. bovis and A. israelii are now
found to be 22% and 77%, respectively, of cases classifiedastwodistinctbacterialspeciesandinnatural
analysed by two molecular techniques (Siqueira & infections the former is restricted to animals and the
Roˆc¸as 2004, Fouad etal. 2005). In this context the latterto humans.
long reported correlation between the prevalence of Human actinomycosis is clinically divided into
enterococci in root canals of primary and retreatment cervicofacial, thoracic and abdominal forms. About
casesandthatinotheroralsites,suchasgingivalsulcus 60%ofthecasesoccurinthecervicofacialregion,20%
and tonsils, of the same patients, is worth noting in the abdomen and 15% in the thorax (Kapsimalis &
(Engstro¨m1964).Theenterococcimaybeopportunistic Garrington1968,Oppenheimeret al.1978).Themost
organismsthatpopulateexposedrootfilledcanalsfrom common species isolated from humans is A. israelii
elsewhereinthemouth(Fouadet al.2005).Therefore, (Wolff & Israel 1891), which is followed by Propioni-
inspiteofthecurrentfocusofattention,itstillremains bacterium propionicum (Buchanan & Pine 1962),
tobeshown,incontrolledstudies,thatE.faecalisisthe Actinomyces naeslundii (Thompson & Lovestedt 1951),
pathogen of significance in most cases of non-healing Actinomyces viscosus (Howell etal. 1965) and Actino-
apicallesionsafterendodontictreatment(Nair2004). mycesodontolyticus (Batty1958) indescending order.
Microbiological (Mo¨ller 1966, Waltimo etal. 1997) Periapical actinomycosis (Fig. 4) is a cervicofacial
andcorrelativeelectronmicroscopic(Nairet al.1990a) form of actinomycosis. The endodontic infections are
studies have shown the presence of yeasts (Fig.3) generally a sequel to caries. Actinomyces israelii is a
in canals of root filled teeth with unresolved apical commensaloftheoralcavityandcanbeisolatedfrom
periodontitis. Candida albicans is the most frequently tonsils, dental plaque, periodontal pockets and carious
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Figure4 Anactinomyces-infectedperiapicalpocketcystaffectingahumanmaxillaryfirstpremolar(radiographicinset).Thecyst
islinedwithciliatedcolumnar(CEP)andstratifiedsquamous(SEP)epithelia.Therectangularblockin(a)ismagnifiedin(c).The
typical‘ray-fungus’typeofactnomycoticcolony(ACinb)isamagnificationoftheonedemarcatedin(c).Notethetwoblack
arrow-headed,distinctactinomycoticcolonieswithinthelumen(LU).Originalmagnifications:(a)·20,(b)·60,(c)·210.From
P.N.R.Nairetal.OralSurgery,OralMedicine,OralPathology,OralRadiologyandEndodontics94:485–93,2002.
lesions (Sundqvist & Reuterving 1980). Most of the 1966,Samantaet al.1975,Weir&Buck1982,Martin
publications on periapical actinomycosis are case & Harrison 1984, Nair & Schroeder 1984, Sakellariou
reports and have been reviewed (Browne & O’Riordan 1996).Althoughperiapicalactinomycosisisconsidered
256 InternationalEndodonticJournal,39,249–281,2006 ª2006InternationalEndodonticJournal
Nair Persistentapicalperiodontitis
to be rare (Nair & Schroeder 1984), it may not be so aetiological factor of persistent apical periodontitis
infrequent (Monteleone 1963, Hylton et al. 1970, followingrootcanaltreatment.Actinomyceshavebeen
Sakellariou 1996). The data on the frequency of shown to posses a hydrophobic cell surface property,
periapical actinomycosis among apical periodontitis Gram-positive cell wall surrounded by a fuzzy outer
lesions are scarce. A microbiological control study coat through which fimbriae-like structures protrude
revealed actinomycotic involvement in two of the 79 (Figdor & Davies 1997). These may help the cells to
endodontically treated cases (Bystro¨m et al. 1987). A aggregate into cohesive colonies (Figdor etal. 1992).
histological analysis showed the presence of Thepropertiesthatenablethesebacteriatoestablishin
characteristic actinomycotic colonies (Fig.5) in two the periapical tissues are not fully understood, but
ofthe45investigatedlesions(Nair&Schroeder1984). appeartoinvolve theability tobuild cohesivecolonies
An identification and aetiological association of the that enables them to escape host defence systems
species involved can be established only through (Figdor etal. 1992). Propionibacterium propionicum is
laboratory culturing (Sundqvist & Reuterving 1980) known to be pathogenic and associated with actino-
ofthe organisms, molecular techniques andbyexperi- mycoticinfections.Butthemechanismofpathogenicity
mental induction of the lesion in susceptible animals of theorganism has not yetbeenexplained.
(Figdor etal. 1992). However, the strict growth
requirements of A. israelii make isolation in pure Otherextraradicular microbes
culture difficult. A histopathological diagnosis has Apical periodontitis has long been considered to be a
generally been reached on the basis of demonstration dynamic defence enclosure against unrestrained inva-
of typical colonies (Nair & Schroeder 1984) and by sionofmicroorganismsintoperiradiculartissues(Kron-
specificimmunohistochemicalstainingofsuchcolonies feld1939,Nair1997).Itis,therefore,conceivablethat
(Sundqvist&Reuterving1980,Happonenet al.1985). microorganismsgenerallyinvadeextraradiculartissues
Today, an unequivocal identification of the organism during expanding and exacerbating phases of the
can be achieved by molecular methods. The charac- disease process. Based on classical histology (Harndt
teristic light microscopic feature of an actinomycotic 1926)therehasbeenaconsensusofopinionthat‘solid
colony is the presence of an intensely dark staining, granuloma’ may not harbour infectious agents within
GramandPASpositive,corewithradiatingperipheral the inflamed periapical tissue, but microorganisms are
filaments (Fig.5) that gives the typical ‘star burst’ or consistentlypresentintheperiapicaltissueofcaseswith
‘ray fungus’ appearance. Ultrastructurally (Nair & clinical signs of exacerbation, abscesses and draining
Schroeder 1984, Figdor etal. 1992), the centre of the sinuses. This has been substantiated by more modern
colonyconsistsofaverydenseaggregationofbranch- correlativelightandtransmissionelectronmicroscopic
ing filamentous organisms held together by an extra- investigations(Nair1987).
cellular matrix (Fig. 5). Several layers of PMN usually However, inthe late 1980s, therewas a resurgence
surround anactinomycotic colony. of the concept of extraradicular microbes in apical
Becauseoftheabilityoftheactinomycoticorganisms periodontitis (Tronstad et al. 1987, 1990, Iwu et al.
to establish extraradicularly, they can perpetuate the 1990, Wayman etal. 1992) with the controversial
inflammation at the periapex even after proper root suggestion that extraradicular infections arethecause
canaltreatment.Therefore,periapicalactinomycosisis of many failed endodontic treatments; such cases
important in endodontics (Sundqvist & Reuterving would not be amenable to a non-surgical approach
1980, Nair & Schroeder 1984, Happonen et al. 1985, but would require apical surgery and/or systemic
Happonen1986,Sjo¨grenet al.1988,Nairet al.1999). medications. Several species of bacteria have been
ActinomycesisraeliiandP.proprionicumareconsistently reported to be present at extraradicular locations of
isolated andcharacterized fromthe periapical tissue of lesions described as ‘asymptomatic periapical inflam-
teeth, which did not respond to proper non-surgical matory lesions…refractory to endodontic treatment’
endodontic treatment (Happonen 1986, Sjo¨gren et al. (Tronstad etal. 1987). However, five of the eight
1988). A strain of A. israelii, isolated from a case of patients had ‘long-standing fistulae to the vestibule…’
failedendodontictreatmentandgrowninpureculture, (Tronstad et al. 1987), a clear sign of abscessed apical
was inoculated into subcutaneously implanted tissue periodontitis draining by fistulation. Obviously the
cages in experimental animals. Typical actinomycotic microbial samples were obtained from periapical
colonies were formed within the experimental host abscesses that always contain microbes and not from
tissue. This would implicate A. israelii as a potential asymptomatic periapical lesions persisting after proper
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Figure5 Periapicalactinomycosis.Notethepresenceofanactinomycoticcolony(AC)inthebodyofahumanapicalperiodontitis
lesion(GR) revealing typical‘starburst’ appearance(inset ina). The transmission electronmicroscopic montage(b) showsthe
peripheralareaofthecolonywithfilamentousorganismssurroundedbyfewlayersofneutrophilicgranulocytes(NG).D,dentine;
ER,erythrocytes.Originalmagnifications:(a)·70;inset·250;(b)·2200.AdaptedfromNair&Schroeder(1984).Printedwith
permissionfromLippincottWilliams&Wilkinsª.
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