R. J. G. DeMoor & A. M. J. C. DeWitte
Department of Operative Dentistry and Endodontology, Dental School, Ghent University, Ghent University Hospital, Gent, Belgium.

Introduction.
Since its introduction to dentistry (Hermann 1920), calcium hydroxide has been widely used in endodontics. Although the overall mechanisms of action are not fully understood, calcium hydroxide nowadays is a widely used endodontic material, thanks to its high alkalinity (Tronstad et al. 1981) and bactericidal effect (Sjogren et al. 1991, Siqueira & Lopes 1999).
In the presence of large and chronic periapical lesions, the deliberate placement of calcium hydroxide beyond the confines of the root canal and into the periradicular tissues has been advocated. Some speculate that it would have a direct effect on inflamed tissue and epithelial cystic linings and in this manner would favour periapical healing and encourage osseous repair (Tronstad et al. 1981). Such deliberate overextension is not, however, widely advocated, since periapical extrusion of calcium hydroxide can have damaging effects. Reports dealing with bone necrosis and continuing inflammatory responses in repaired mechanical perforations (Himel et al. 1985), the neurotoxic effects of root canal sealers (Boiesen & Brodin 1991), cytotoxicity on cell cultures (Alacam et al. 1993), damaged epithelium with or without cellular atypia when applied on hamster cheek pouches (Dunham et al. 1966), cellular damage following early calcium hydroxide dressing of avulsed teeth (Andreasen & Kristerson 1981) and necrosis of buccal gingiva and mucosa after periradicular overextension due to alkaline burn (De Bruyne et al. 2000) have been presented.
The aim of the present evaluation was, therefore, to review a number of case histories in our clinic, dealing with accidental and voluminous calcium hydroxide overextension and to evaluate the impact of these on periapical healing (especially for those cases with immediate active flare-ups).

Reports.
A clinical and radiographic retrospective evaluation was made of 12 teeth in 11 patients. The follow-up varied between 1.5 and 8 years after calcium hydroxide placement. An overview of the cases is given in Table 1.
The case histories consisted of nine incisors with a history of trauma and three cases with a history of pulp necrosis. Pulp necrosis was associated with a large coronal restoration and cusp fracture in a mandibular premolar, an extensive composite filling on a maxillary lateral incisor and a leaking porcelain crown on a maxillary central incisor. For those teeth without sinus tracts, periapical lesions were detected after radiographic evaluation. In all cases, it was decided to conventionally treat the root canals. Anaesthesia was provided when sensitivity was reported during preparation of the access opening (one case ) or during root canal treatment (two cases). The root canals were cleaned and shaped with Flexofiles (Dentsply/Maillefer, Ballaigues, Switzerland) in balanced force motion and according to the step-back technique. A 2.5% sodium hypochlorite solution was used to rinse the canals. After drying with sterile paper points, a calcium hydroxide paste [Reogan-Rapid (Vivadent, Schaan, Liechtenstein) or Calxyl (Otto and Co., Frankfurt, Germany)] was placed as an intermediate dressing. With Reogan-Rapid, an injection technique was used. With Calxyl, a lentulo spiral was used to introduce the paste into the canal. Excess material was removed from the pulp chamber with curettes. A sterile cotton pellet was placed in the pulp chamber, and glass ionomer cement (Ketac-Fil, Espe, Seefeld, Germany) provided the temporary coronal seal. In each case, the radiograph revealed unintentional extrusion of calcium hydroxide paste beyond the confines of the root canal into the periradicular lesion. The patients reporting slight pain and tenderness during the placement of calcium hydroxide paste were those with more than half of the apical lesion filled. In three cases where a fistula was present, calcium hydroxide paste entered the course of the fistula. Here, no pain was reported whilst placing the calcium hydroxide.
Patients were then seen on consecutive appointments depending on the symptomatology of the teeth. At their second appointment, half (6 out of 11) of the patients reported that they had slight-to-severe and diffuse pain the day after the placement of calcium hydroxide, and most of them (9 out of 11) reported a mild, diffuse intraoral swelling of the buccal mucosa. Pain generally decreased within the next 2 days. There were two patients with pain lasting more than 2 days. One patient (patient 2; Table 1) complained of severe pain and an extraoral swelling after 1 day. This case history will be discussed in detail. A second patient (patient 8; Table 1) was seen suffering from pain and diffuse swelling of the buccal mucosa after 2 days. The endodontically treated mandibular premolar was also mobile. The root canal was irrigated with 2.5% sodium hypochlorite and then dried with paper points. A new calcium hydroxide dressing was not placed. The root canal was sealed with a sterile cotton pellet and Ketac-Fil (Espe) and the occlusion relieved. Ibuprofen 600 mg (Brufen Forte, Knoll NV., Brussels, Belgium) as well as an antibiotic, Amoxicillin 500 mg (Clamoxyl, Smith Kline Beecham, Genval, Belgium), were prescribed. The tooth was free of symptoms after another 2 days.

Table 1. Case reports of unintentional calcium hydroxide overextensions.

All patients in the present evaluation (except for patients 2 and 8; Table 1) were seen after 1 week. In these cases where swellings were reported, it was also seen that it took more than 1 week for these swellings to disappear. The calcium hydroxide dressings were, in general, renewed at the second visit. The root canals were finally obturated in each case with gutta–percha and AH26 (Dentsply/DeTrey, Konstanz, Germany) using cold lateral gutta–percha condensation in the third visit. In patients 2 (Case 1), 10 (Case 2) and 11, the calcium hydroxide dressings were renewed twice due to continuing exudation and the permanent root fillings were performed at the fourth visit.
Follow-up, up to 8 years, after the initial calcium hydroxide placement, revealed symptom- free teeth. The radiographic examinations gave evidence of healing of the periradicular lesions. Calcium hydroxide was only resorbed in eight of the 12 teeth. All fistulas disappeared within 1 month, but it took more than 6 months for all periradicular radiolucencies to disappear.

A 14-year-old male patient (Table 1; patient 2) was seen for the first time for a routine dental examination. There was a history of dental trauma to the right maxillary central incisor (tooth 11; FDI), i.e. a crown fracture without pulp exposure at the age of nine and a restoration with a composite. A routine periapical radiograph revealed the presence of a periradicular lesion in association with teeth 11 and 12 (Fig. 1). Furthermore, apical root resorption was associated with teeth 11, 21 and 22 probably due to an earlier orthodontic treatment, though inflammatory resorption following trauma and pulp necrosis could not be ruled out. Out of all the four incisors, only tooth 11 did not respond to cold and heat, and showed a negative response to the electric pulp test. Tooth 11 was opened without anesthesia and root canal treatment was started. The root canal was dry and there was no apical exudation. After cleaning and shaping (MAF 80), Reogan-Rapid was injected into the root canal using the injection needle as provided by the manufacturer. During injection, the patient complained of pressure around the root apex. The control radiograph showed that the periapical lesion was filled with calcium hydroxide paste (Fig. 2). The next day the patient suffered from severe pain and a swelling of both buccal mucosa and upper lip. After 2 days, the pain as well as the extraoral swelling disappeared spontaneously. The intraoral swelling, however, remained. It was decided not to open the root canal and to postpone further treatment for 1 month. At the third appointment, it was not possible to completely dry the root canal and a new calcium hydroxide dressing was placed. Due to the open apex associated with the apical root resorption, an additional amount of calcium hydroxide was unintentionally added to the periapical mass (Fig. 3). This time there were no symptoms of pain and swelling.
The calcium hydroxide paste was refreshed after another month. The tooth remained asymptomatic, though the buccal mucosa was still sensitive to palpation. Care was taken not to introduce the new dressing into the periradicular region (Fig. 4). On the control radiograph (Fig. 4), it was seen that there was a white border surrounding the periapical lesion, with a diminished amount of periradicular calcium hydroxide. Finally, 3 months after initial consultation, the root canal was prepared to a MAF 90 and obturated by cold lateral condensation of gutta–percha and AH 26 (Fig. 5). On the 1-year control radiograph, remnants of the calcium hydroxide dressing were visible in the periradicular region and the periapical lesion was notcompletely healed (Fig. 6).The 4-year control radiograph showed evidence of healing, though there was a white zone present embedded in the bone (Fig. 7).

Figure 1. Radiograph of the right central incisor with periapical radiolucency. Apical root resorption on both maxillary incisors is probably the result of orthodontic therapy.



Figure 2. Radiograph after placement of an intracanal calcium hydroxide dressing with unintentional periapical overextension.



Figure 3. Radiograph taken after renewal of the calcium hydroxide dressing 1 month after the start of endodontic therapy. An additional amount of calcium hydroxide was unintentionally added.



Figure 4. Radiograph taken after a second replacement of the calcium hydroxide paste, 2 months after the start of endodontic therapy.



Figure 5. Control radiograph of the root canal obturation, 3 months after initial consultation. The extraradicular calcium hydroxide had disappeared.



Figure 6. The 1-year control radiograph. There are still remnants of the calcium hydroxide paste. The size of the apical radiolucency is diminishing.



Figure 7. The 4-year control radiograph showing healing of the apical lesion and the presence of a white radiopaque spot at the place where calcium hydroxide remnants were originally present.

A 22-year-old male patient (Table 1; patient 10) was seen with the complaint of tooth mobility, tooth discolouration and loss of tooth substance of both maxillary central incisors. There was a history of a trauma 4 years previously with extensive crown fractures. Apical radiolucencies were present on teeth 11 and 21 (Fig. 8). No signs of an active fistula was seen. Endodontic treatment was started in tooth 11. The root canal was cleaned and shaped up to a MAF 100. Reogan-Rapid paste was introduced in the root canal. The paste was also unintentionally extruded into the periradicular region and into an undiagnosed sinus tract, entering the buccal fold. (Fig. 9). The excess of calcium hydroxide paste was removed using a moistened gauze and the soft tissues were vigorously rinsed with saline. Seven days later tooth 21 was cleaned and shaped up to a MAF 100 and a calcium hydroxide intracanal dressing was placed. As the sinus tract was still present, the root canal was thoroughly cleaned and copiously irrigated with sodium hypochlorite 2.5%. The dressing in tooth 11 was renewed. The patient returned after 10 months (due to postponement of appointments) and the permanent root filling of tooth 21 was performed (Fig. 10). As the sinus tract was still present, tooth 11 was cleaned and shaped up to a MAF 110 and a new calcium hydroxide dressing was placed. On the control radiograph, (Fig. 10) the apical radiolucency associated with tooth 21 had apparently disappeared. There was still an overextension of calcium hydroxide at the apex of tooth 11. One month later, the fistula was absent, though it was not possible to completely dry the root canal. A new calcium hydroxide dressing was placed. A diminished periapical radiolucency was seen on the control radiograph as well as the remnants of the calcium hydroxide paste (Fig. 11). The permanent root canal filling of tooth 11 was performed 1 year and 4 months after the first visit, again due to postponed appointments. Both apical radiolucencies had disappeared. The remnants of the more than 1-year old calcium hydroxide overextension were still present, but these remnants apparently did not disfavour apical healing (Fig. 12). The 2-year control radiograph confirmed healing of the lesion, with remnants of the calcium hydroxide paste still present (Fig. 13).

Figure 8. Detail of an intraoral radiograph, showing periradicular radiolucencies on both maxillary central incisors, with a history of untreated dental trauma.



Figure 9. Control radiograph of the calcium hydroxide dressing with unintentional periradicular overextension into the buccal fold through a sinus tract.



Figure 10. Control radiograph of the root canal obturation of tooth 21. As the sinus tract was still present, the calcium hydroxide paste was renewed in tooth 11. Due to postponement of appointments, there was a difference of 10 months between the first session (Fig. 8) and the present root canal fillings.



Figure 11. Control radiograph of another calcium hydroxide replacement 1 month after the previous 10 months appointment. There is still calcium hydroxide present in the periapex.



Figure 12. Control radiograph of the permanent root canal filling of tooth 11 and showing healed periapical lesions of both teeth 11 and 21. There are still remains of the previously overextended calcium hydroxide paste.



Figure 13. The 2-year control radiograph. The periradicular situation remains unchanged.

Discussion.
It has been demonstrated that treatment with calcium hydroxide as an interim dressing in the presence of large and chronic periapical lesions can create an environment more favourable to healing and encourage osseous repair (Cvek 1972, Heithersay 1975, Vernieks & Messer 1978, Sahli 1988, Caliskan & Sen 1996). Nonetheless, despite the acknowledgement of calcium hydroxide as one of the most effective antimicrobial dressings during endodontic therapy, its antibacterial activity remains controversial and it is not clear whether the benefits of this substance are based solely upon superior antibacterial activity (Siqueira & Lopes 1999). Extension of the material beyond the apex has, therefore, been advocated by some to benefit from:

1. anti-inflammatory activity, neutralization of acid products, activation of the alkaline phosphatase and antibacterial action (Souza et al. 1989);
2. destruction of the epithelium thereby allowing the connective tissue invagination into the lesion (Sahli 1988).

The present evaluation was undertaken after we encountered an alkaline soft tissue burn due to a severe overextension into the periradicular tissues (De Bruyne et al. 2000). In order to evaluate the effect of known excessive overextensions of calcium hydroxide (half and more of the lesion filled) on the healing and periradicular repair of large periapical lesions, the clinical records of the patients attending our clinic with apical periodontitis during the last 10 years were consulted. Of the 11 case histories found with calcium hydroxide overextensions, nine were associated with clinical symptoms of swelling and pain lasting for at least 2–4 days after calcium hydroxide placement. Despite these flare-ups, all cases showed successful periradicular repair. Repair was associated with complete resorption of the extruded paste and ultimate periapical healing in more than half of the cases in the present study. In five cases, however, complete resorption of the paste (Reogan-Rapid) did not occur, although the periradicular and peri-extrusion radiolucency disappeared. A possible explanation for the complete resorption of Calxyl paste may be that the paste does not contain barium sulphate (which is added to calcium hydroxide pastes to improve radiopacity), whereas Reogan-Rapid does (Fava & Saunders 1999). Furthermore, a general finding was that in the present cases of extensive calcium hydroxide overextension, repair took more than 6 months to be complete. This finding confirms the findings of Vernieks & Messer (1978) who suggested that extrusion of calcium hydroxide beyond the apex may be a cause for the lack of early healing of periapical lesions. In this respect, there remains contradiction with other investigators who have advocated that direct contact between calcium hydroxide and periapical tissues is beneficial for osseoinductive reasons (Ghose et al. 1987, Rotstein et al. 1990). Finally, the present data confirm our previous conclusion on damage of the gingival and mucosal tissues induced by alkaline burn (De Bruyne et al. 2000), that as long as there is no intimate and prolonged contact of calcium hydroxide paste with soft tissues, reactions remain mild and are of transient nature.

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