J Clin Periodontol 2002: 29: 781–783 Copyright C Blackwell Munksgaard 2002Printed in Denmark . All rights reserved

0303-6979

Case Report

Stefano Sartori, Maurizio SilvestriEndoperiodontal lesion and Vitaliano Cattaneo

UDA Periodontology & Maxillofacial Surgery,S. Matteo Hospital, Pavia, ItalyA case report

Sartori S, Silvestri M, Cattaneo V. Endoperiodontal lesion. J Clin Periodontol2002; 29: 781–783. CBlackwell Munksgaard, 2002.

AbstractThe purpose of this case report is to present an unusual endoperiodontal lesionon tooth 46 in an 8-year-old child. The absence of any carious process and thepresence of the typical radiographic aspect of an infrabony defect, led us to con-sider the periodontal aetiopathogenesis. In spite of all this, an accurate peri-

Key words: endoperiodontal lesion;odontal probing of all the teeth and the use of the pulp tester for teeth 46 andperiapical lesion; pulp necrosis36 led us to diagnose properly a truly endodontic lesion. The endodontic treat-

ment of the involved tooth achieved the complete healing of the lesion. Accepted for publication 23 May 2001

Introduction

Apical foramina and accessory root ca-nals can lead to the transmission of aninfection from the endodontic spaces tothe periodontium and vice versa. Everytime dentine is exposed to the oral en-vironment, pulp reacts with a defensiveinflammatory reaction. In fact, when atooth is involved by a carious processor restorative procedures, oral bacteriaor their components can arrive at thepulp via dental microtubules. Often inthese cases, some typical signs of a peri-odontal involvement can be observed.In addition to thermal hypersensitivity,pain caused by percussion, a slight en-largement of the periapical periodontalspace may be radiographically detected(Langeland 1987). If dental pulp doesnot degenerate into a necrotizing pro-cess, it reacts by producing reparativedentine and, after removal of the aeti-opathogenetic factor (e.g. carioustissue), symptoms and periapical radio-graphic signs should disappear.

Pulp necrosis is always associatedwith a periapical response and its na-ture, as many studies have demon-strated, is microbiological (Bergenholtz1974, Sundqvist 1976). After an initialphase in which the pathologic phenom-enon expands itself from the apical partof the pulp to the periapical tissue, the

second phase may evolve in two poss-ible ways: the formation of an acute ab-scess or the establishment of a balancebetween the bacterial challenge and thehost response (Yu & Stashenko 1987,Stashenko & Yu 1989). This balanceconsists of an inflammatory processthat leads to the formation of a richlyvascularized granulation tissue, whichis infiltrated by different inflammatorycells (Stashenko 1995, Nair 1987, Mar-ton & Kiss 1993). The inflammatorytissue may stay the same size for manyyears or can increase, sometimes be-coming a cystic lesion. An abscess mayarise every time the balance betweenbacteria and the host breaks down. Theradiographic aspect of the periodontalresponse to the pulp necrosis and bac-terial contamination consists of an areaof radiolucency generally localised inthe proximity of the apical foramen orsometimes the accessory lateral endo-dontic canals. Lateral canals containvessels and connective tissue. The widthof lateral canals is reduced by continu-ous deposition of dentine and root ce-mentum, which could explain why lat-eral endodontic lesions are more fre-quent in young permanent molars withinfected pulp than in the molars ofadults. Many authors have studied thelocation and the frequency of lateral ca-nals in permanent teeth, finding the

highest concentration in the apical partof the root and at the furcation level(Lowman et al. 1973, Burch & Hulen1974, Koenigs et al. 1974, Vertucci &Williams 1974, De Deus 1975, Gut-mann 1978). Periapical acute manifes-tations due to canal infections can in-crease in size, causing a progressive de-struction of the periodontal apparatus.If this lesion evolves into an abscess thesuppurative exudate tries to find adrainage to the gingival sulcus (or peri-odontal pocket), generally through theperiodontal ligament or perforating thebone wall and running, in this last case,along the soft tissues. When the endo-dontic infection drains through theperiodontal ligament, a typical narrowand deep probing site can be detectedor, rarely, as in the reported followingcase, an unusual extensive destructionof the periodontal tissue. Even in thislatter case, if the origin of the lesion istruly endodontic, a proper endodontictreatment will lead to a complete heal-ing of the periodontal tissues.

Case report

An 8-year-old male was referred to ourattention for a deep pocket (16mm)(Fig.1) all along the buccal and distalaspect of the 46. The absence of anycarious process was verified, the pulp

782 Sartori et al.

Fig. 1. A 16 mm probing depth at time 0.

Fig. 2. Tooth 46 at time 0 after the cavity test.

Fig. 3. Four months after the treatment withCa(OH)2.

tester and the cavity test confirmed thevitality of the tooth but with a slightlyinferior response with respect to the 36.A wide periodontal defect involving thefurcation (Fig.2) could be observedradiographically at the distal aspect ofthe mesial root (except 1mm apically)and the bone around the distal root, ex-cept for its most apical portion. Nodeep caries or fractures had been de-tected and the history had not revealedany traumatic injuries in the past fewyears.

For these reasons one of the diagnos-tic hypotheses was a periodontal lesion.This diagnosis was reinforced by thetypical morphology of the defect, thewide extension of the probing site allalong the buccal and distal aspect of the

Fig. 4. Eight months after Ca(OH)2 appli-cation.

Fig. 5. Eight months after the final endodon-tic treatment.

Fig. 6. Probing depth of 5 mm 8 months afterthe final endodontic treatment.

tooth, the absence of deep caries andthe positivity of the pulp tester and cav-ity test.

The probing of all the other primaryand permanent teeth revealed probingdepths �3mm. The pulp tester appliedto tooth 46 revealed a slightly inferiorresponse compared to tooth 36. There-fore another diagnostic hypothesis waspartial pulp necrosis of a not wellknown nature, involving the most co-ronal portion of the pulp, which couldhave promoted the periodontal involve-ment through the wide lateral canalspresent in such young patients, espe-cially at the furcation level (Lowmanet al. 1973, Burch & Hulen 1974, Ko-enigs et al. 1974, Vertucci & Williams1974, Gutmann 1978). In spite of the

unclear nature of this supposed endo-dontic lesion, we decided to perform anendodontic treatment.

The first step in our therapeutic planwas initially to promote the apex for-mation by means of Ca(OH)2. Afteropening the pulp chamber, the non-vi-tal pulp tissue was removed and the en-dodontic spaces were shaped by NickelTitanium instruments (LightspeedA??)and washed out with a sodium hypo-chlorite 5% solution. After an accuratedrying of the canals they were filledwith a pure Ca(OH)2 powder. Fourmonths later (Fig.3), we could detect apartial apex closure and a reduction ofthe lesion. It was decided to wait an-other 4months. Eight months later(Fig.4), apex formation was completedand the original lesion disappeared. Itwas decided to perform the final endo-dontic treatment by filling the endodon-tic spaces with vertically condensed gut-tapercha. Eight months after the treat-ment (Fig.5), complete healing of theperiodontal tissues could be seen. Atthis time, the probing attachment level(PAL) was 5mm (Fig.6) with a PALgain of 11mm. No periodontal treat-ment was performed.

Conclusions

The morphology of the bone defect de-tected in the X-ray and the probingdepth measured all along the buccaland distal aspect of the involved toothseemed to indicate a diagnosis of theperiodontal origin of the lesion. How-ever, the pulp vitality test, the history ofthe patient and the healthy periodontalstate of all the other teeth strongly sup-ported the endodontic nature of the de-fect. Following endodontic treatmentwith an appropriate healing period, thePAL gain and the filling of the defectdetected by X-ray confirmed the purelyendodontic origin of the lesion.

This case report demonstrates that acorrect diagnosis is necessary for se-lecting the best treatment plan and foravoiding over-treatment.

Zusammenfassung

Der Zweck dieses Fallberichtes ist die Dar-stellung einer ungewöhnlichen endoparodon-talen Läsion an Zahn 46 bei einem 8 Jahrealten Kind. Die Abwesenheit jeglicher kariö-sen Läsion sowie das typische röntgenologi-sche Bild eines infraalveolären Defekts führ-ten ursprünglich zur Annahme einer paro-

Endoperiodontal lesion 783

dontalen Ätiopathogenese der Läsion.Nachdem die Erhebung von Sondierungs-parametern an allen Zähnen nur an Zahn 46erhöhte Werte und Sensibilitätstests an Zahn46 eine im Vergleich zu Zahn 36 verzögerteReaktion ergeben hatten, wurde die Diagno-se einer primär endodontalen Läsion gestellt.Allein die Wurzelkanalbehandlung von Zahn46 führte zu einer vollständigen Ausheilungdes Defektes.

Resume

Le but de ce rapport de cas etait de presenterune lesion endo-parodontale inhabituelle surune 46 chez un enfant de 8 ans. L’absencede tout processus carieux et la presence d’unaspect radiographique typique d’un defautintra-osseux nous a conduit a considerer uneetio-pathogenie parodontale. En depit detout cela, un sondage parodontal precis dechaque dent et l’utilisation d’un pulp-testersur les dents 46 et 36 ont permis de diagnosti-quer vraiment une reelle lesion endodonti-que. Le traitement endodontique des dentsimpliquees entraına la guerison complete dela lesion.

References

Bergenholtz, G. (1974) Micro-organismsfrom necrotic pulp of traumatized teeth.Odontologisk Revy 25, 347–358.

Burch, J. G. & Hulen, S. (1974) A study ofthe presence of accessory foramina andthe topography of molar furcations. OralSurgery 38, 451–455.

De Deus, Q. D. (1975) Frequency, location,and direction of the lateral secondary andaccessory canals. Journal of Endodontics 1,361–366.

Gutmann, J. L. (1978) Prevalence, locationand patency of accessory canals in the fur-cation region of permanent molars.Journal of Periodontology 49, 21–26.

Koenigs, J. F., Brilliant, J. D. & Foreman, D.W. (1974) Preliminary scanning electronmicroscope investigations of accessory for-amina in the furcation areas of human mo-lar teeth. Oral Surgery 38, 773–782.

Langeland, K. (1987) Tissue response to den-tal caries. Endodontics and DentalTraumatology 3, 149–171.

Lowman, J. V., Burke, R. S. & Pelleu, G. B.(1973) Patent accessory canals: incidencein molar furcation region. Oral Surgery36, 580–584.

Marton, I. J. & Kiss (1993) Characterizationof inflammatory cell infiltrate in dentalperiapical lesions. International Endodon-tic Journal 26, 131–136.

Nair, P. N. (1987) Light and electron micro-scopic studies of root canal flora and peri-apical lesions. Journal of Endodontics 13,29–39.

Stashenko, P. (1995) Reduction of infection-

stimulated periapical bone resorption bythe biological response modifier PGG glu-can. Journal of Dental Research 74, 323–330.

Stashenko, P. & Yu S. M. (1989) T-helper andT suppressor cell reversal during the devel-opment of induced rat periapical lesions.Journal of Dental Research 68, 830–834.

Sundqvist, G. (1976) Bacteriologic studies ofnecrotic dental pulps. Umea UniversityOdontological Dissertation .7.

Vertucci, F. J. & Williams, R. G. (1974) Fur-cation canals in the human mandibularfirst molar. Oral Surgery 38, 308–314.

Yu S. M. & Stashenko, P. (1987) Identifi-cation of inflammatory cells ion develop-ing rat periapical lesions. Journal of Endo-dontics 13, 535–540.

Address:Dr Stefano SartoriVia Scalabrini næ 9 3129100 PiacenzaItaly

Tel: π39 328 9773427Fax: π39 0523 314248e-mail: stefano.sartori/unipv.it