|Year : 2014 | Volume
| Issue : 2 | Page : 105-108
Necrosis of gingiva and alveolar bone caused by accidental sodium hypochlorite seepage during endodontic treatment
GS Sajjan1, CD Dwarakanath2, N. V. D. Nalam1, Satya Kalyani Singamsetty1
1 Department of Conservative Dentistry and Endodontics, Vishnu Dental College, Bhimavaram, West Godavari District, Andhra Pradesh, India
2 Department of Periodontics and Implantology, Vishnu Dental College, Bhimavaram, West Godavari District, Andhra Pradesh, India
|Date of Web Publication||15-Oct-2014|
G S Sajjan
Department of Conservative Dentistry and Endodontics, Vishnu Dental College, Bhimavaram, West Godavari District, Andhra Pradesh
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Sodium hypochlorite is an effective intracanal irrigant when used judiciously with rubber dam isolation. Inadvertent contact of sodium hypochlorite may lead to severe necrosis of soft tissue. A case of gingival and alveolar bone necrosis caused by accidental leakage of sodium hypochlorite under the rubber dam during root canal preparation was reported. After initiation of root canal treatment, during the second visit patient complained of pain in the gingiva surrounding the tooth. Accidental seepage of hypochlorite into gingiva and underlying bone led to the necrosis of these tissues. The patient required surgical intervention which led to successful recovery.
Clinical Relevance To Interdisciplinary Dentistry
- Sodium hypochlorite (NaOCl), the widely used irrigant in Endodontics has many complications following it inadvertent use
- Necrosis of soft tissues and underlying alveolar bone is a rare, potential complication after NaOCl irrigation that requires an interdisciplinary approach
- Teamwork of periodontists, endodontists and prosthodontists is important for the successful management of such complications.
Keywords: Alveolar bone necrosis, gingival necrosis, root canal treatment, sodium hypochlorite
|How to cite this article:|
Sajjan G S, Dwarakanath C D, Nalam N, Singamsetty SK. Necrosis of gingiva and alveolar bone caused by accidental sodium hypochlorite seepage during endodontic treatment. J Interdiscip Dentistry 2014;4:105-8
|How to cite this URL:|
Sajjan G S, Dwarakanath C D, Nalam N, Singamsetty SK. Necrosis of gingiva and alveolar bone caused by accidental sodium hypochlorite seepage during endodontic treatment. J Interdiscip Dentistry [serial online] 2014 [cited 2021 Sep 18];4:105-8. Available from: https://www.jidonline.com/text.asp?2014/4/2/105/142952
| Introduction|| |
Sodium hypochlorite (NaOCl) is the most widely used irrigant in endodontic treatment as it is effective against a broad spectrum of microorganisms, dissolves necrotic tissue and has lubricating properties. It is used as an adjunct to mechanical debridement of root canals during endodontic treatment.  It is used in varying concentrations ranging from 0.5% to 5.25% depending upon the dilution and individual preferences. With the increase in concentration the tissue dissolving property and antibacterial activity increases along with its cytotoxic property.  One of the major drawbacks with NaOCl is its ability to cause acute inflammation when it is in direct contact with vital tissues, and this may further lead to necrosis.  Many case reports described the potential complications following extrusion periapically, seepage through lateral perforations, accidental injection into the maxillary sinus, paraesthesia, accidental splashing into eyes and chemical burns of the skin. ,,,,,,,, The most common of these complications is its extrusion into the periapical tissues. Few reports were also presented on its hypersensitivity reactions. ,,
This report presents a case in which accidental seepage of hypochlorite into the soft tissues caused its necrosis, followed by necrosis of underlying bone.
| Case report|| |
The 33-year-old female patient reported to the Post Graduate Department of Conservative Dentistry and Endodontics, with a chief complaint of pain in her lower right back tooth for the past 10 days. Her medical history was noncontributory, and past dental history revealed the extraction one of her lower tooth 2 years back. Extraoral findings were within the normal limits.
Intraoral examination revealed presence of deep dentinal caries and gingival recession in tooth no. 47. On palpation of the buccal and lingual mucosa apical to the tooth no tenderness was observed. The tooth was negative for the percussion sensibility. Vitality tests were carried out by thermal and electric pulp tester. Periapical radiograph showed disto-proximal radiolucency involving enamel, dentin, and pulp [Figure 1]a]. A final diagnosis of irreversible pulpitis was made, and root canal treatment was initiated.
|Figure 1: (a) Preoperative intraoral periapical radiograph (IOPAR).(b) Sloughing of gingiva on buccal side.(c) Sloughing of gingiva on lingual side.(d) IOPAR on the second visit when sloughing of gingiva was observed.(e) Necrosed bone on lingual side.(f) After removal of sequestrated bone, repositioned fl ap with interrupted sutures.(g) Sequestrated bone sent for histopathological examination.(h) Immediate postobturation IOPAR.(i) Postcementation buccal view of Metal FPD.(j) Postcementation lingual view of FPD.(k) Immediate post cementation of FPD IOPAR.(l) Eosin and hematoxylin staining of histopathological section showing empty osteocytic lacunae and necrosed bone loss of trabecular pattern|
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After administration of local anesthesia and rubber dam isolation, the access cavity was prepared, and pulp extirpation was done. Lost distal surface was developed with a composite restoration. Working length (WL) determination was done with electronic apex locator (Root ZX, J.Morita, USA) and intraoral periapical radiographs. Biomechanical preparation was done with hand Ni-Ti K-files (Dentsply Maillefer, Ballaigues, Switzerland) up to ISO size 35 in all the canals along with intermittent irrigation of 3% sodium hypochlorite (Prime Dental Products Pvt. Ltd., Thane, India) and was temporarily restored with Coltosol (Coltene-Whaledent, Langenau, Germany).
Patient complained of pain in the gingiva surrounding tooth no. 47 during the second visit. On examination, sloughing of gingiva was observed on both the buccal and lingual surfaces [Figure 1]b and c]. Patient was immediately referred to Department of Periodontics where removal of composite restoration was advised, and necrosed soft tissue was excised. The underlying bone was visible and adjacent gingiva was appreciably healthy. Periodontal pack was placed, and excised soft tissue was sent for histopathological examination. The histopathological report confirmed the necrosis of gingival connective tissue.
In the subsequent visit necrosis of bone was observed on the buccal and lingual surfaces [Figure 1]e]. Flap elevation was done from the lingual surface, and necrosed bone was removed. This was followed by repositioning of the flap with interrupted sutures [Figure 1]f]. Antibiotics (Amox 500, Ranbaxy Laboratories Limited, Barotiwala, India) and antiinflammatory drugs (Combiflam, Sanofi India Limited, Ankleshwar, India) were prescribed for 5 days. Necrosed bone was sent for histopathological examination, and it was confirmed as Sequestrated bone [Figure 1]g]. In the follow-up visit, patient was asymptomatic, healing was observed, and sutures were removed. In the same visit, obturation was done by lateral compaction technique with Zinc oxide eugenol sealer (Dental products of India, Mumbai, India) and Gutta-percha [Figure 1]h]. In the next visit postendodontic restoration was done.
Patient was referred to Department of Prosthodontics for replacement of missing tooth no. 46. Metal fixed partial denture was fabricated and cemented with teeth no. 45 and no. 47 as abutments [Figure 1]i and j]. The clinical and radiographic follow-up showed favorable healing. During 1-year follow-up the patient was asymptomatic; clinically there was healthy gingiva surrounding tooth no. 47. Radiographically bone formation was evident in the furcation area and on the distal surface of tooth no. 47 [Figure 1]k].
| Discussion|| |
Sodium hypochlorite an effective irrigant in various concentrations has many serious complications after its inadvertent use. Of that inadvertent extrusion into periapical tissues is the most common.  Extrusion of the solution into periapical tissues may occur in teeth with wide apical foramina or when the apical constriction has been damaged during the biomechanical preparation.  Application of excessive pressure during irrigation, binding of the needle in a constant position, placing the needle tip up to the WL or using needles with smaller gauges may deliver the irrigant into the periapical tissues. 
The immediate squeal includes sudden, severe excruciating pain of 2-5 min duration which may be related to the tissue destruction, distension, periapical tissue bleeding and immediate swelling which may increase for few days.  The caustic effects of sodium hypochlorite are because of its high alkalinity (pH = 10.8-12.9) and hypertonicity that causes oxidation of proteins.  In high concentrations, severe necrosis was also observed. Heling et al. reported that sodium hypochlorite concentrations >0.01% are lethal to fibroblasts in vitro.  In addition to its toxic effects, hypochlorite has an unpleasant odor and causes damage to clothing on contact. 
Management of complications initially should include the application of cold compresses on the 1 st day. From the 2 nd day, it should be replaced with warm compresses and warm mouth rinses to stimulate the local microcirculation. To reduce the acute pain, local anesthetics in association with the prescription of analgesics might be helpful. Intravenous steroids have also been recommended in some cases. In mild symptoms, antibiotics are not necessary. In cases with moderate to severe symptoms antibiotics are prescribed to minimize the risk of secondary infections. ,,
In the present case, accidental seepage of NaOCl solution into the gingival soft tissue surrounding tooth no. 47 occurred during irrigation of the root canals. This accidental seepage had occurred due to of the presence of Class-I gingival recession. As rubber dam was placed during the treatment, seepage was unnoticed resulting in the necrosis of gingiva and underlying bone. Patient didn't experience pain during the seepage of NaOCl solution probably because of anesthesia.
In teeth with gingival recession application of provisional restorative material such as Cavit G (3M ESPE Germany) which hardens with moisture  can be done to seal the rubber dam around the tooth. Application of petroleum jelly prior would also be beneficial to prevent the contact of irrigating solutions to soft tissues in areas of gingival recession. The histopathology report of soft tissue showed necrosis of epithelium and underlying fibrous connective tissue with a focal area of necrosis. The histopathology report of decalcified section of bone showed empty lacunae with no evidence of osteoblastic rimming suggestive of Sequestrated bone [Figure 1]l]. Necrosis of tissues occurred because of the tissue dissolving property of NaOCl and hypertonicity of the solution that caused the injury primarily by oxidation of proteins.
Rubber dams are mainly used during endodontic treatment for protection of the patient from aspiration, isolation from saliva and provision of focus on the treatment location. Hence, it is considered as the most useful equipment for isolation of the operating field in Endodontics. Placement of the dam properly, positioning the clamps and frames accurately help us to obtain leakage free configurations and prevent further complications. The main factor that contributed to the accident in this case was the gingival recession that was not sealed before the rubber dam application. During endodontic treatment, rubber dam should be placed to isolate the tooth and any minor defects during adaptation should be corrected with a caulking agent to optimize the seal.
In this case diagnosis and immediate treatment by surgical intervention have led to a favorable outcome.
| References|| |
|1.||Pontes F, Pontes H, Adachi P, Rodini C, Almeida D, Pinto D Jr. Gingival and bone necrosis caused by accidental sodium hypochlorite injection instead of anaesthetic solution. Int Endod J 2008;41:267-70. |
|2.||Spencer HR, Ike V, Brennan PA. Review: The use of sodium hypochlorite in endodontics - potential complications and their management. Br Dent J 2007;202:555-9. |
|3.||Crincoli V, Scivetti M, Di Bisceglie MB, Pilolli GP, Favia G. Unusual case of adverse reaction in the use of sodium hypochlorite during endodontic treatment:A case report. Quintessence Int 2008;39:E70-3. |
|4.||Sabala CL, Powell SE. Sodium hypochlorite injection into periapical tissues. J Endod 1989;15:490-2. |
|5.||Gatot A, Arbelle J, Leiberman A, Yanai-Inbar I. Effects of sodium hypochlorite on soft tissues after its inadvertent injection beyond the root apex. J Endod 1991;17:573-4. |
|6.||Ehrich DG, Brian JD Jr, Walker WA. Sodium hypochlorite accident: Inadvertent injection into the maxillary sinus. J Endod 1993;19:180-2. |
|7.||Kavanagh CP, Taylor J. Inadvertent injection of sodium hypochlorite into the maxillary sinus. Br Dent J 1998;185:336-7. |
|8.||Linn JL, Messer HH. Hypochlorite injury to the lip following injection via a labial perforation. Case report. Aust Dent J 1993;38:280-2. |
|9.||Herrmann JW, Heicht RC. Complications in therapeutic use of sodium hypochlorite. J Endod 1979;5:160. |
|10.||Ingram TA 3 rd . Response of the human eye to accidental exposure to sodium hypochlorite. J Endod 1990;16:235-8. |
|11.||Serper A, Ozbek M, Calt S. Accidental sodium hypochlorite-induced skin injury during endodontic treatment. J Endod 2004;30:180-1. |
|12.||Hülsmann M, Hahn W. Complications during root canal irrigation-literature review and case reports. Int Endod J 2000;33:186-93. |
|13.||Kaufman AY, Keila S. Hypersensitivity to sodium hypochlorite. J Endod 1989;15:224-6. |
|14.||Caliskan MK, Türkün M, Alper S. Allergy to sodium hypochlorite during root canal therapy: A case report. Int Endod J 1994;27:163-7. |
|15.||Heling I, Rotstein I, Dinur T, Szwec-Levine Y, Steinberg D. Bactericidal and cytotoxic effects of sodium hypochlorite and sodium dichloroisocyanurate solutions in vitro. J Endod 2001;27:278-80. |
|16.||Witton R, Brennan PA. Severe tissue damage and neurological deficit following extravasation of sodium hypochlorite solution during routine endodontic treatment. Br Dent J 2005;198:749-50. |
|17.||Summitt JB, Robbins JW, Hilton TJ, Schwartz RS. Fundamental of Operative Dentistry: A Contemporary Approach. 3 rd ed. Illinois: Quintessence Books; 2006. p. 179. |