Ⅰ. INTRODUCTION

Sodium hypochlorite is among the most commonly used irrigants in endodontic treatment due to its antimicrobial activity and ability to dissolve organic tissue [1]. Its mechanism of action involve formation of hypochlorous acid and chloramines which disrupt bacterial metabolism and cause irreversible oxidation of essential enzymes [2]. In addition, the solution’s high alkalinity promotes saponification of fatty acids and neutralization of amino acids, leading to liquefaction of organic debris and reduced surface tension, there- by enhancing its tissue-dissolving capacity [3]. While the dissolution of necrotic tissue within the confines of root canal system contributes to effective root canal disinfection, inadvertent contact with vital tissues may lead to severe adverse effects.

Possible causes of sodium hypochlorite accidents include both anatomical and procedural factors that facilitate the unintended extrusion of the irrigant beyond the root canal system. These may involve structural disruptions such as destruction of the apical constriction or perforation of the canal walls, as well as mechanical factors like the wedging of the irrigation needle within the canal [4]. In addition, the presence of fenestrations or dehiscence in the cortical bone, an active sinus tract, or direct communication with the maxillary sinus can serve as pathways for irrigant leakage into surrounding tissues [5]. Sodium hypochlorite accidents have also been reported to occur more frequently in maxillary teeth and in female patients, possibly due to anatomical factors such as thinner and less dense cortical bone [6].

There have been several case reports of sodium hypochlorite accidents, as well as literature reviews discussing their symptoms, causes, and management strategies, often with suggestions for clinical guidelines. However, detailed serial documentation of soft tissue changes through clinical observation remains limited. This case report documents the immediate tissue response and healing progression through serial clinical photographs taken at multiple time points, with continued follow-up over approximately three months. To the best of our knowledge, this is one of the few case reports to provide such comprehensive temporal documentation of a sodium hypochlorite accident.

Ⅱ. CASE REPORT

A 66-year-old female patient presented with the chief complaint of “I want to receive treatment because of severe cavities. I also feel that my gums have receded significantly.” She had a medical history of undergoing surgery for endometrial cancer approximately six years prior. Clinical and radiographic examinations revealed multiple carious lesions. Notably, the mandibular left lateral incisor (#32) exhibited significant attrition and buccal cervical caries, accompanied by a buccal sinus tract. A gutta-percha cone tracing of the sinus tract led to the apex of tooth #32 (Fig. 1a). The tooth was tender to percussion and palpation. Periapical radiography showed a well-defined radiolucent lesion at the apex of tooth #32 (Fig. 1b). Based on these findings, the tooth was diagnosed with chronic apical abscess, dental caries, and attrition. Non-surgical root canal treatment was planned for tooth #32.

After obtaining informed consent from the patient, local anesthesia was administered using lidocaine containing epinephrine. A rubber dam was placed for isolation. The access cavity was prepared through the bucco-incisal attrition surface of tooth #32, and non-vital pulp tissue was extirpated. The working length was determined to be 17 mm using a Root ZX (J. Morita, Kyoto, Japan) apex locator, and canal patency was confirmed. Canal instrumentation was performed up to a #25 K-file, and irrigation was carried out using 2.5% sodium hypochlorite (NaOCl). Approximately two minutes after irrigating the canal with 1 mL of NaOCl, the patient suddenly complained of acute pain in the right and left mandibular premolar area. Upon removal of the rubber dam, intraoral examination revealed swelling, redness, and warmth extending from the left canine (#33) to the right lateral incisor (#43) in the labial vestibule and lower lip. Bleeding from the sinus tract was noted, along with a mucosal opening in the vestibular area. The surrounding mucosa was covered by a thin epithelial layer but showed whitish discoloration and softening, suggestive of underlying tissue liquefaction and subepithelial necrosis (Fig. 2a). No significant extraoral changes were observed at that time. Immediate irrigation of the root canal and sinus tract with 30 mL of sterile saline was performed. The canal was dried with paper points, medicated with calcium hydroxide, and temporarily sealed with Caviton (GC Corporation, Tokyo, Japan). The patient was prescribed prednisolone (5 mg, three times daily for 3 days), and a 7-day regimen of amoxicillin/clavulanic acid (625 mg, three times daily), metronidazole (250 mg, twice daily), aceclofenac (twice daily), and 0.12% chlorhexidine mouthwash (twice daily).

On the following day (Day 1), the patient returned, reporting that she had experienced a headache until the previous night, but had no specific symptoms at the time of the visit. Extraoral examination revealed ecchymosis in the lower premolar region of the chin, bilaterally. Intraorally, swelling of the lower lip and chin was noted along with a mucosal opening of similar size to that observed on the previous day (Fig. 2b). Copious irrigation of the root canal and sinus tract was performed with 30 mL of sterile saline, followed by medication with calcium hydroxide. The access cavity was temporarily sealed with Caviton. Additional saline irrigation and topical dressing with Hibitane were performed on the lower buccal vestibular area. A follow-up visit was scheduled in three days.

At the third visit (Day 5), the patient reported that her discomfort had subsided, though mild tenderness remained in the left lower chin. Extraoral examination showed resolving ecchymosis, with only scattered spots remaining as traces. Intraorally, the mucosal opening had extended with yellowish discoloration and fibrin-like tissue consistent with liquefactive necrosis (Fig. 2c). The same irrigation and dressing procedure as the previous visit were repeated. At the fourth visit (Day 7), the patient reported no significant discomfort. Extraoral ecchymosis had completely resolved. Intraorally, the area of exposed liquefactive necrosis exhibited focal zones of yellowish granular tissue, resembling saponified fat, suggestive of fat necrosis and enzymatic tissue destruction (Fig. 2d). Tooth #32 was partially tender to percussion, but non-tender to palpation and negative on bite test, with no mobility. Root canal instrumentation was extended using a ProTaper Next X3 NiTi file (Dentsply Sirona, Ballaigues, Switzerland), followed by copious irrigation with 20 mL of saline. Calcium hydroxide was placed as intracanal medicament, and the cavity was sealed with Caviton. Additional saline irrigation and vestibular dressing were performed.

One week later (Day 14), the patient remained asymptomatic. The mucosal opening had gradually closed, and partial fibrotic transformation and re-epithelialization were noted intraorally (Fig. 2e). The buccal sinus tract had resolved, and tooth #32 elicited no pain upon percussion, palpation, or bite testing. Cone Beam Computed Tomography (CBCT) was performed to assess the cause of NaOCl extrusion and to evaluate surrounding anatomical structures. The imaging revealed a periapical lesion with buccal bone fenestration associated with tooth #32 (Fig. 3). Routine saline irrigation and intracanal dressing were carried out.

Another week later (Day 21), the patient had no symptoms. Intraoral examination revealed that the immature fibrous tissue had matured into dense, scar-like connective tissue, indicating ongoing tissue remodeling (Fig. 2f). Root canal obturation was completed using gutta-percha and EndoSeal MTA (Meta Biomed, Cheongju, Korea). At the nine-week follow-up after obturation (Day 84), the initially firm, scar-like tissue had softened and become more pliable, blending well with the adjacent mucosa in both texture and color (Fig. 2h). This was interpreted as normalization of collagen organization and resolution of the acute fibrotic response. The patient remained asymptomatic and radiographic images also showed decrease in periapical lesion size (Fig. 4).

Ⅲ. DISCUSSION

This case report presents a sequential documentation of the acute tissue response and progressive healing over a twelve-week period following a sodium hypochlorite accident. Initially, a mucosal opening with signs of tissue liquefaction and necrosis was observed intraorally, while bilateral ecchymosis developed on the chin by the following day. The intraoral necrotic area expanded over the first week, and by Day 7, features of fat saponification and fat necrosis were evident. During the second and third weeks, the affected area began to show fibrotic transformation and re-epithelialization, with dense scar-like tissue formation. By the twelfth week, the scar tissue had softened and blended with the adjacent mucosa, indicating resolution of fibrosis and reorganization of collagen.

When sodium hypochlorite comes into contact with vital tissues, hypochlorous acid, a strong oxidizing agent, can cause hemolysis of red blood cells, skin ulceration, and cellular injury in endothelial cells and fibroblasts. It may also inhibit neutrophil migration, impairing local immune responses [7, 8]. In addition, hydroxide ions contribute to cellular dehydration and lipid saponification, leading to liquefactive necrosis. Residual alkali can penetrate deeper into soft tissues, causing further elevation of local pH and exacerbating tissue destruction [9]. These biochemical reactions collectively result in extensive protein denaturation, enzymatic degradation, and fat saponification, which explain the intraorally observed tissue liquefaction and mucosal opening observed in this case. The extraoral ecchymosis likely resulted from damage to capillary endothelium and subcutaneous tissue hemorrhage induced by chemical injury and inflammatory vascular leakage [10].

The healing process observed in this case closely followed the typical phases of wound healing that occur after chemical injury to oral soft tissues. During the first week, the affected area remained in an inflammatory-proteolytic stage. Polymorphonuclear neutrophils dominated the first 24-48 hours, releasing reactive oxygen species and proteases that liquefy necrotic debris. By 48–72 hours, macrophages replaced neutrophils, clearing the digestate through phagocytosis and secreting cytokines and growth factors to initiate repair [11]. Granulation tissue formation was likely underway, with new blood vessels and fibroblasts migrating into the fibrin scaffold. The yellow discoloration and apparent lesion enlargement observed around one week may reflect ongoing inflammation and fat saponification associated with the tissue breakdown. The extensive liquefactive necrosis produced by NaOCl may correspond histologically to a zone of protein denaturation, surrounded by acute inflammation and early reparative changes such as angiogenesis [12].

From the second to the third week, fibroblasts proliferate and deposit a loose network of type III collagen, while basal keratinocytes migrate beneath the fibrin clot to re-epithelialize the wound surface [13]. Oral mucosa, in contrast to skin, exhibits faster epithelial closure and reduced inflammatory response, which may explain the relatively rapid fibrotic transformation and minimal scar formation observed in this case. By the twelfth week, matrix metalloproteinases have remodeled the provisional extracellular matrix, replacing most type III collagen with more organized and cross-linked type I collagen fibers. As myofibroblast activity subsides, the scar tissue softens and integrates with the surrounding mucosa, which indicates the hallmarks of the late remodeling phase [14].

One potential contributing factor to the sodium hypochlorite accident in this case is the presence of a buccal bone fenestration. A CBCT scan taken on Day 14 revealed that the periapical lesion surrounding the apex of tooth #32 had caused localized bone resorption, resulting in a fenestration of the buccal cortical plate (Figure 3). The absence of apical resistance due to surrounding bone loss may predispose the site to irrigant extrusion, as even minimal increases in irrigation pressure, often unrecognized by the operator, can lead to a sodium hypochlorite accident [15]. In fact, CBCT-based studies have found that such cortical defects may significantly increase the risk of irrigant extrusion. In a cross-sectional clinical study by Souza et al., all teeth involved in NaOCl accidents exhibited direct communication between the apex and buccal soft tissue through a cortical bone fenestration, whereas no such fenestrations were observed in the control group [16]. A more recent retrospective CBCT analysis by Cho-Kee et al. further confirmed that cortical bone fenestrations were present in 100% of affected cases, while iatrogenic perforations were identified in only 19%, reinforcing fenestration as a major anatomical risk factor [17].

However, bone fenestration alone does not account for the accident. Procedural factors likely contributed alongside high-risk anatomical features to the extrusion of sodium hypochlorite. The pulpal and periapical status, specifically the presence of non-vital pulp and a well-defined periapical lesion, may have further increased the risk. The absence of pulp tissue may render the root canal a low-resistance pathway, facilitating irrigant extrusion [18]. Furthermore, while intact periapical tissues provide resistance through back pressure and limited compliance, helping to prevent sodium hypochlorite extrusion, the presence of a periapical lesion can reduce this resistance, thereby facilitating irrigant escape. Once extruded, the lesion may retain the irrigant and allow it to diffuse into adjacent tissues, increasing the risk of chemical injury [19].

Management of sodium hypochlorite accidents requires prompt recognition and supportive care to minimize tissue damage and prevent secondary complications. Immediate measures include copious irrigation with sterile saline to dilute and remove residual irrigant, thereby reducing the intensity of acute tissue reactions [20]. Analgesics should be administered to manage post-incident pain, and corticosteroids may be considered to control the inflammatory response. Acetaminophen-based analgesics are most commonly prescribed, while nonsteroidal anti-inflammatory drugs (NSAIDs) are also used [21]. Glucocorticosteroids contribute to pain relief by suppressing inflammatory responses and modulating mediators involved in pain development. Systemic antibiotics are also recommended to prevent or control secondary infection, especially in cases involving extensive soft tissue damage or mucosal openings [22, 23].

Regular follow-up and repeated intraoral dressing with antiseptics such as chlorhexidine or Hibitane can help maintain a clean wound environment, promote epithelialization, and minimize the risk of delayed healing or tissue breakdown [24]. In the present case, sodium hypochlorite extrusion was promptly recognized and managed with immediate saline irrigation, systemic corticosteroids, antibiotics, and analgesics. Repeated intraoral dressing with antiseptics and calcium hydroxide medication supported local wound control and disinfection. The mucosal necrosis gradually resolved with re-epithelialization and tissue remodeling observed over follow-up. No long-term complications were noted, and radiographic healing of the periapical lesion was confirmed.

In conclusion, sodium hypochlorite accidents may result from a combination of anatomical vulnerabilities, such as buccal bone fenestration, and procedural factors that facilitate irrigant extrusion beyond the root canal system. These accidents typically provoke immediate tissue reactions, including mucosal breakdown, liquefactive necrosis, and fat saponification, which then undergo a sequential healing process. Recognizing the characteristic patterns of tissue injury and recovery is important for distinguishing normal healing from pathological changes, thereby enabling timely and appropriate clinical intervention when healing does not proceed as expected.