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Fjiilod Diiil rmiimuliil I<)'>1>: 12:

I'rinli'fl ill Druiiuirh • ,-\U ii^lii\ irs


d Muiiksgiiard

I »96

Endodontics & Dental Traumatology

ISSS (Il(l'>-2^(I2

Case report

Periapicai actinomycosis: report of a case and review of the literature

Sakellariou PL, Periapicai aclinoniycosis: lepcirl ol a case and re- view of the lileiatiue, Endod I^enl Traumatol 1996; 12: 151-154, © Munksgaard, 1996

Abstract - This case of )3eriapical actiuomycosi.s presented the clinical pictttre of chronic periapicai inllammation. The diagno- sis was based on die histological examination ol the periapicai le- sions suggesting the necessity for routine histological exatnina- lion. Although root canals pro\ide a piimai)' jDort ol entry the Acti)iomyfe.s orgcXnisuK into the periapicai tisstte, periapicai actin- omycosis, is considered exlremcly rare. This ma)- be due to the omission of rotitine histological examination oi peria])ical le- sions and the clinical l^ehavior of the disease. The large nutiiber of cases reported dtiring tlie last decade itidicates that periapicai actinomycosis is moi e freqtient than what it is believed and lliis is important in the daily denial practice.

P, L, Sakellariou

Athens, Greece

Key words: actinomycosis: periapicai actinomycosis: periapicai inflammation: periapicai infection

Piiiiip Sai<enarioLi, 31 Diligianni St., f45 62 Kifissia, Afliens, Greece

Accepted October 2.1995

The maiti etiological agent ol htiman actinomyco-

sis is Aciinoinyces israelii, followed by Aradmia }>roj)i- onica, A. naeslundU, A. atid A. odoniolyticus

in descending order (1-S), Th e aclinomya's are normal saptophytes iti the oral cavity. The patho- genesis of actinomycosis is not clear. It is believed, however, that actinomyces enter the tissues follow- ing trauma and become pathogenic (4), The ttstial location of actinc:)mycosis is the cetvi- cofacial region in 60% of cases, followed by the ab- dotninal in 20%, thoracic in 15% (5) and the cere- bral in 5% (6), Periapicai actinomycosis is consid- ered extremely rare (3), Aciinomycps are found in 10,6 to 17,2 of infected root canals (7, 8) which are tlie primary port of entry for Actinomyces organisms into the periapicai tissue, Hardwick & Newman (9), atid Villa (10) liave found colonies of Actinomyces in the pulp cham- beis of teeth with cornual absesses. Howevet; tlie largest number of cases reported to date, arc of ac- tinomycosis of i^etiapical granttloiiias. Weir & Buck (11) report a case of periapicai ac- tinomycosis and in reviewing the literattiie ttntil 1982 they found 20 cases includiug dieir own.

A teview of the literatttre from 1982 till now re- veals 25 additional cases including the present one, A series of 16 cases is teported by Happonen et al, (1, 2), The diaguc:>sis was conlhmed bv ini- mtitiocytochemical histologica! examination of the periapicai lesions in which the presence of ,4r- tinomyces israelii atid in descetiditig order A. propi- onicadwA A. iiaesluiidriwere fbuud. Two cases were t eported by Nair c*v: Schroedcr (3) in a histological examination of 45 cases of periapicai lesions, Perna et al, (6) report one case of actitiomycotic granuloma of the right Gasserian ganglioti, with the primary site an actinomycotic periapicai gran- uloma of the right thiid inferior molar. Five iso- lated cases are reported by Martin & Harrison (12), Craig et al, (13), Nishimura (14), O'Grady & Reade (15), Figttres & Dottgias (16), Review of the literature shows that the cases of periapicai actino- tnycosis teported until toda)' total 45 inchtding this one. The purpose of this study was to show tJiat th e pei-iapical actinomycosis, a disease that may cavise serious complications (6), is involved in the aiea of the dentist's dailv practice and is not extremely rare, as is commonlv believed.




Ritdiograp h

showin g

hug e

coiilinuou s

nidiolucenc y

roo t ca -

alon g ih e upict- s o f -1."), -Ki an d 17 an d lli f nals lining ollli c molars.

inconipki c

Case report

A 56-year old while man was referred with tbe

diagnosis of peria|)ical cyst of tbe right mandible. Twenty days prior to the rcleiTal the ]3atient devel- oped a .swelling of tlie liglil mandibular vestibule. The swelling was redueed wilhin a week with anti- biotic treatment (tetracycline 250 mg four times a day for 10 days) ]3rescribed by the denlist. Tlie patient had an tnireniarkable medical history. On examiniition the swelling had disappeared and palpation of ilu- right mandibtilar vestibule was painless and listula tree.

The radiograpiis (Fig. 1-2) revealed a large ra- diolucent ])eriai3icii! area extending from the apex

ol 47 to and including the apex of 45. Teeth 46

and 47 showed incomplete filling of the root ca-

nals. Tooth 45 was non-caritjus and did not le-

I'iir. 2. t^aleral ladiogiapl i o l th e righ t mandible , showin g Ih e

liinils o/ ih c ladiohn ein




spond to eiectrie and diermal pulp testing. Tbe

teeth weie slightly sensitive to percussion. Tlie pa- tient had never before complained oi diseotnfort from this area or leported any injuries. Tine lesion was operated Ijased on the radiological diagnosis of iniected periapical cyst. Undei- inferior dental nerve block anesthesia, an incision was made along the nuicogingival junction from 47 to 45. A mucoperiosteal flajj was reflected and the cortical bone was exposed. Tbe cortical bone corresjDonding to the apex of 46 was papyraceous witb a j^erfbration of 1 mm. The per- foration was enlarged atid revealed the entire cav- ity. Teeth 47, 46 and 45 were extracted and a gran- ular tnass which filled the etitire periapical cavity and was not attached to the bone was removed. The flap was stUured with silk, a rubl^er dam drain

on a l egime of

500 nig penieifliu three times a day for 6 days. The next day tlie drain was remo\ed and the suttnes were removed on tlie 6th ]5ost-operative day. The liealingwas uneventful. As the histological examination revealed actinomycosis, tbe admini.s- tration of peiiieillin was prolonge d for two addi- tional weeks. The histologieal examination (Fig. 3) of tlie ma- terial from tbe pei iapical fesions consisted of gran- ular tisstie with dense inflammatory infiltration composed of polymorphonuclear leucocytes, some lymphocytes and many plasma cells (3). The sttrface was partly tilcet ated an d pat tly covered by fiyi)er]3fastic squamous epithelium without celfu- lai- atypia. Among exudative elements some typical colonies of actinoniyces were present. Diagnosis:

inserted aud the patient was placed

"periapical actinomycosis".

Radiographs taken three years after oiJeration showed cotnplete regenetation of the bone in the peria])icaf region (Fig. 4); 5 years postopei atively there was no sign of recttrrence.


This case presented the clinical picture of usual chronic jjeriapical inflammation. Tbe diagnosis was accidental from the histological exatninatioti of the periapical lesion, in which tfie characteristic colonies of the cictinomyce.s constituted an uncontroveisiaf proof of actinomycosis. Tbe farge osteolytic periapical area (Fig. 1, 2) sttggested that the symptomless disease had been piesent for a long time before the recent exacerbatioti. In the jaws actinomycosis may occur as a central fesion or it may occur in the soft tissue arottnd the niatidi- ble. In the central type of actinomycosis of tbe jaw, as in the present case, the bone destruction may exist for a long time liefore symptoms appear; fre-

Fis;. 3. l'hotoniiero<;ta|)h ol ti.s.stie .seclion showitig colony ol actinoniycete.s .stirtouiuled In inllaniniatory cells. (I Ieiiiatoxv- lin atid eositi staiti X 2.'iO).

qucnll y it i.s by roenlgc n diagnosi. s llia t a n o.steitic defecl is discovered which, when ojjeraled npon, proves lo be due to aclinoniycosis (4). hi such cases lhe soft tissues are not necessarily involved (4). The .syniptoniless clinical bahavior in the present case suggested tlial the aetiitotnyres are of low virulence. These organisms also lack tissue decomposing enzymes (hyaluronidases) and so require the aid of other partly aerobic, partly anaerobic noti-specillc bacteria, particularly sta- phyloroeei and streptoeoeei lo achieve ]3alhogenecily (5). In addition, these organisms may establish au eqtiilibiitim with the tissue without necessar- ily causing an acute resjjonse or undue discomlbrt to the host (3). In the present case, as in most pre\ious cases of periapical actiuomycosis, the diagnosis followed endodontic. In this case, the diOerence was treat-

of the right tiiandible, thtee years alter O|>

eration, .showiiij; cotiiplete tegetietation of the bone in the

periapical region.

h'ig. 4. Radiogtapli

Periapical actinomycosis

ment lhat the endodontic therapy had been per- ibrmed se\eral years ago without the patient hav- ing complained ever since. The exacerbation ap- peared 20 da)s prior to the referral. Withotit ex- cluding the possibility of hematogenic spreading to an already established periapical lesion, the most propable wa)' for aetinoittyre.s to be introciticed to the periapical region is through the root canal. Unfortunately, in this case, as in all pi e\dous cases, we do not know whether the artiuornyees were in- tiodticed before the endodontic therapy or were advanced as a result of stich tlierap). We know, however, that endodontic therapy alone fails in cases of periapical lesions in which actinomycosis is in\ olved. In such cases surgical cm ettage of the periapical lesion is recjuired too (1, 11). It is strange that the periapical actinomycosis is considered extremely larc^ since the root canals provide the primar\' port of entry for the Aetinomy- TM organisms inlo the periapical tissues. In the cei- vicofacial actinomycosis which accotmts for 60% of all cases, the clinical picture is very obviotis:

.swelling, itidttration of soft tissues, abscesses, draining sinuses and fislulae. With this clinical pic- lure, it is essential for lhe clinician to suspect ac- tinomycosis and look for the laboiatoi)- proof of the disease in the pus of the abscesses and fistiilae. On the contrary, in the periapical actinomycosis the clinical picture is at)pical, as in the present case, and it is confused with the tisual and more freqtient chronic periapical inflammations. Rotitine microscopy periapical lesions, espe- cially tliose which resist endodontic theiap)' may lead lo a re\ised understanding of the occurrence of actinomycosis in periapical lesions. This re- search may be done also with the help of inmiuno- cytochemical histological methods (1, 2, 17), which identify the species oi' aetiitoinyee.sdnd reveal small colonies that are not morphologically char- acteristic and are easily oxeiiooked in routine his- topathological examination (2). This is supported by the impressive series of 16 cases of periapical actinomycosis reported by Happonen et al. (1,2) and by the reported 2 cases of periapical actino- mycosis by Nair & Schroeder (3) in histological ex- amination of 45 cases of periapical lesion, while thoiLsands of periapical lesions are encountered daily without histological examination. Tlie belief tliat "a tootli with a granulotna may have an infected root canal, but a sterile periapical tisstie" (18, 19) pre\'ailed fbr nian\' years and stopped the microbiological research of periapical lesions, because such a tesearch was consideied to be done in vain. However, the presence of colo- nies of (letiitomyces in periapical lesions, as in the present case (Fig. 3), and other microorganisms



(20-22), changed tlic bcliel that pciiapical lesions arc free o( microorganisms and proved that ticlino- mycc.s s])ecies and other microorganisms may stir- vive in periapical lesions. As a result, the signiiicancc of the lact that mi- croorganisms are incltided and stirvive in the liv- ing tissues of the periapical lesions and not only in tlic dead and inaccessible to the circulation root canal mtisl be Itirther considered and cvahiated.


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L ,



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