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Necrosis of the Gingiva Caused by Calcium

Necrosis of the Gingiva Caused by Calcium

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Published by Dr.O.R.GANESAMURTHI

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Published by: Dr.O.R.GANESAMURTHI on Mar 15, 2011
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CLINICAL ARTICLE
Necrosis of the gingiva caused by calciumhydroxide: a case report
M. A. A. De Bruyne
1
, R. J. G. De Moor
1
& F. M. Raes
2
1
Department of Operative Dentistry and Endodontology; and
2
Department of Fixed Prosthodontics and Periodontology, DentalSchool, University Gent, Gent, Belgium
AbstractDe Bruyne MAA, De Moor RJG, Raes FM.
Necrosis of the gingiva caused by calcium hydroxide: acase report.
International Endodontic Journal,
33,
67±71,2000.
Case report
The present case demonstrates the possibledetrimental effect of an overextension of a calcium hydroxideintracanal dressing into the periradicular and soft tissue afteriatrogenic buccal root perforation of a maxillary centralincisor.At first this perforation was not recognized by the dentist,which resulted in the introduction of a large amount of non-setting calcium hydroxide paste under the gingival tissuesthrough a dehiscence on the buccal side of the root.This report describes the consequences and management of the necrosis of the buccal gingiva and mucosa, and thesubsequent treatment and follow-up of the root perforation.
Keywords
:
calcium hydroxide, glass ionomercement, necrosis, perforation, surgical repair.
Received 14 October 1998; accepted 5 March 1999
Introduction
Since its introduction in dentistry, calcium hydroxide(Ca(OH)
2
) has been used for a wide variety of purposesincluding lining of cavities, indirect and direct pulpcapping, dressing after pulpotomy, dressing of the rootcanal between appointments, prevention of rootresorption, repair of iatrogenic perforations, treatment of horizontal root fractures and as a constituent of root canalsealers (Foreman & Barnes 1990). Few reports deal withthe negative side-effects of Ca(OH)
2
, that include bonenecrosis and continuing inflammatory response inrepaired mechanical perforations (Himel
et al 
. 1985), theneurotoxic effect of root canal sealers (Boiesen & Brodin1991), cytotoxicity on cell cultures (Ala
cË
am
et al 
. 1993),damaged epithelium with or without cellular atypia whenapplied on hamster cheek pouches (Dunham
et al 
. 1966)and cellular damage following early calcium hydroxidedressing of avulsed teeth (Andreasen & Kristerson 1981).The following report describes the deleterious effects of Ca(OH)
2
inacaseofiatrogenicrootperforation.
Case report
A 27-year-old Caucasian male was referred by hisdental practitioner to the emergency clinic for furtherendodontic treatment of his maxillary left centralincisor. The patient presented with a swollen upper lipand, on clinical inspection, an extensive necrotic zoneon the buccal side of 21 and 11 was noted (Fig. 1).Tooth 21 was not painful on percussion.From the dental history it was clear that the practi-tioner had commenced the root canal treatment1 week earlier. Since the pulp chamber and thecoronal part of the root canal were obliterated withdentine, the dentist had difficulty locating the canal.Various radiographs were taken but these did notshow any evidence of incorrect angulation of the filecompared with the long axis of the tooth and themesiodistal location of the root canal (Fig. 2a,b). A
q
2000 Blackwell Science Ltd International Endodontic Journal,
33,
67
±  
71, 2000
Correspondence: Dr Mieke A. A. De Bruyne, Department of OperativeDentistry and Endodontology, Dental School, University Gent, DePintelaan 185 P8, 9000 Gent, Belgium.
67
 
provisional root canal preparation was performed,using 2.5% NaOCl as a canal irrigant. No intracanaldressing was placed. In a second session the final rootcanal shaping was done. As it was difficult to obtain adry canal, an interappointment calcium hydroxidedressing was placed (Control; pH = 12, la maisondentaire, Balzers, Switzerland). Unfortunately, theradiograph of this dressing (Fig. 3) revealed a largeamount of material extruded through the root.One day later, the upper lip was swollen and 2 dayslater the gingiva showed sudden perforation in thisarea. The patient experienced no pain. For 2 weeks thenecrotic gingival zone was treated with rinses of hydrogen peroxide 3% and chlorhexidine 2% in wateronce every 2 or 3 days. During this time a regimen of daily application (BID) of chlorhexidine digluconate10 mg g
1
gel (Corsodyl gel; Smith Kline Beecham,Genval, Belgium) was also prescribed. The gingivalperforation healed and closed completely within2 months (Fig. 4). Two millimeters of gingivalrecession measured from the cemento-enamel junctionresulted. A surgical endodontic intervention wasplanned, but postponed by the patient for 6 months.At this surgical treatment session all temporaryfilling material in the access cavity was removed. Asthe introduction of a file in the apical part of the rootcanal was complicated by the palatal inclination of thetooth crown and the presence of an extensive mid rootledge, it was decided to combine surgery and rootcanal preparation in one session.
Figure 1
Necrotic gingiva extending from tooth 21 to11.
Figure 2
(a, b) Radiographs showing no evidence of incorrect angulation of the file compared with the long axis of the tooth and the mesiodistal location of the root canal.
Figure 3
Radiograph of the interappointment calciumhydroxide dressing.
International Endodontic Journal,
33
, 67
±  
71, 2000
q
2000 Blackwell Science LtdCa(OH)
2
induced gingival necrosis
De Bruyne et al.
68
 
Under local anaesthesia a full thickness flap wasraised. Following flap reflection, a pronounced bonydehiscence was observed. The buccal side of themidroot had been perforated. The buccal opening inthe root facilitated the visualization of the location of the opening of the apical part of the root canal. Aftercleaning, shaping and root canal obturation with coldlateral gutta percha condensation and AH26 (DeTrey,Konstanz, Germany), the buccal perforation was closedwith glass ionomer cement (Ketac-Fil; Espe, Seefeld,Germany) (Figs 5 and 6). At this time scar tissue fromthe healing soft tissues and the periosteum were cutthrough to mobilize the flap. The root surface wasconditioned with saturated citric acid (pH = 1) for1 min. The flap was repositioned coronally and closedwith GoreTex sutures (W. L. Gore & Associates, Inc.,Flagstaff, Arizona, USA). Compression of the flap wascarried out and the access cavity filled with Ketac-Filglass ionomer cement (Espe, Seefeld, Germany).Ten days later sutures were removed and thesurgical area cleaned; healing was uneventful (Fig. 7).At the three-month recall the tooth was free of clinicalsymptoms and the patient had no complaints. Thebuccal gingival recession measured from the cemento-enamel junction was limited to 1 mm. At 6 monthsthe maximum probing depth was 3 mm, indicatingthat the periodontal intervention had resulted in a newattachment over the treated root. Radiographicexamination revealed a normal status (i.e. absence of any periapical or periodontal pathology) and thegingival recession remained stable (Fig. 8a,b).
Discussion
The initiation and stimulation of mineralization, the anti-bacterial characteristics and the dissolution of necroticmaterial are the main indications for the extensive use of 
Figure 4
Healed buccal mucosa after 2 months.
Figure 5
Radiograph of the completed root filling.
Figure 6
Closure of the perforation with glass ionomercement.
Figure 7
Operation site after 10 days.
q
2000 Blackwell Science Ltd International Endodontic Journal,
33,
67
±  
71, 2000
De Bruyne et al.
Ca(OH)
2
induced gingival necrosis
69

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