0099-2399/91/1700-0038/$02.00/0 JOURNAL OF ENDODONTICS Copyright 9 1990 by The American Association of Endodontists
Printed in U.S.A. VOL. 17, NO. 1, JANUARY1991
CASE REPORT Thermally Induced Pulpalgia in Endodontically Treated Teeth Daniel M. Keir, DDS, William A. Walker III, BS, DDS, MS, William G. Schindler, DDS, MS, and Steven E. Dazey, DMD
Two cases of thermally induced pulpalgia in teeth previously endodontically treated are presented. Reproduction of the patient's chief complaint was the key to identifying the teeth involved. In both cases, the pulpalgia was stimulated by heat. After locating and treating an unfilled canal, the teeth have remained asymptomatic. Possible explanations for this occurrence are discussed.
defects were noted. Radiographically, there was no evidence of periapical involvement and the canal obturation appeared to be adequate (Fig. 1). Endodontic diagnostic tests were performed first with cold using a cotton pellet saturated with skin refrigerant (dichlorodifluoroethane). Teeth 29 and 31 were responsive to cold when stimulated on the facial surface, with no lingering or throbbing pain while tooth 30 was nonresponsive. All teeth responded normally to percussion and palpation. Each tooth was then isolated with a rubber dam and stimulated with 155~ water. Teeth 29 and 31 were normally responsive to heat. Tooth 30 responded immediately with intense pain that continued as a dull ache which the patient identified as her chief complaint. Tooth 30 was anesthetized and isolated with a rubber dam. After access was made, the gutta-percha in the distal canal was removed with a G P X (Brasseler USA, Inc., Savannah, GA). Careful exploration of the distal canal area revealed an unfilled D F canal. The canal was totally debrided and prepared with a circumferential step-back flare technique and 5.25% NaOC1 irrigation. After completion of instrumentation, the D F and DL canals appeared to merge as one broad distal canal. The canal was dried, a nonmedicated cotton pellet was placed in the pulp chamber, and the access opening was closed with Cavit (Premier Dental Products Co., Norristown, PA). The patient was seen 2 days later and had a mild apical periodontitis, but no longer complained of thermal sensitivity. The tooth was isolated with a rubber dam and stimulated with hot water as before with no response. The distal canal was obturated with laterally condensed guttapercha and Roth's 801 sealer (Roth International, Ltd., Chicago, IL), and the access opening was closed with IRM (L. D. Caulk Division, Dentsply International Inc., Milford, DE) (Fig. 2). The patient was referred for final restoration of #30. Two days later the tooth was completely comfortable and has remained so for several months.
The most challenging aspect of many endodontic cases is the diagnostic gymnastics involved in identifying the tooth that is the etiology of the patient's pain rather than the debridement and obturation of the canal space. The ability to reproduce, alter, or eliminate the patient's chief complaint is of significant importance in this process. Various means such as thermal stimulation, percussion, palpation, and selective anesthesia may be useful in accomplishing this. Although toothache caused by thermal stimulation is commonly associated with teeth containing vital, inflamed pulps, it is u n c o m m o n to encounter this in endodontically treated teeth. The purpose of this article is to report on two cases involving a toothache stimulated by heat. In both cases, the thermally sensitive teeth had been previously treated endodontically. CASE 1 A 38-yr-old female complained of prolonged pain on the lower right side which occurred when she drank or ate something hot. She identified tooth 30 as the sensitive tooth. It had been endodontically treated 9 months earlier because of a chief complaint of lingering sensitivity to cold and biting sensitivity. Following this treatment her chief complaint had been eliminated. The tooth subsequently was restored with a M O D F L gold onlay. The patient indicated that her sensitivity to heat began after the onlay was cemented. Examination of the mandibular fight posterior teeth revealed that teeth 29 and 31 were restored with class 2 amalgam restorations and #30 with a M O D F L onlay. All restorations had intact margins with no recurrent caries. No periodontal
CASE 2 A 50-yr-old female presented with a complaint of severe pain on the lower left side which was stimulated by heat. She identified # 17 as the source of her pain. Teeth 18 to 21 were missing and tooth 17 had been treated endodontically 11 months earlier for prosthodontic expediency (Fig. 3). It had 38
Vol. 7, No. 1, January 1991
Pulpalgia following Endodontic Treatment
F=G 1. Case 1, radiograph of initial endodontic treatment.
FIG 3. Case 2, radiograph of initial endodontic treatment.
FIG 2. Case 1, radiograph following retreatment of distal canal.
FiG 4. Case 2, radiograph at 15 months following treatment of MF canal.
been asymptomatic and normally responsive to thermal stimulation at the time of treatment. During endodontic treatment, only two canals were located and treated. It was subsequently restored with an amalgam core buildup and a gold crown and served as an abutment for a mandibular RPD. Tooth 17 was isolated with a rubber dam and stimulated with hot water, reproducing the severe pain. The tooth was anesthetized, access was made, and the gutta-percha was removed from the pulp chamber. Careful exploration of the pulp chamber floor revealed an untreated M F canal. The canal was debrided and prepared using a circumferential step-back flare technique and 5.25% NaOC1 irrigation. The canal was dried, a nonmedicated cotton pellet was placed in the pulp chamber, and the access opening was closed with an IRM temporary restoration. At the next appointment 2 wk later, the patient was asymptomatic. The tooth was isolated with a rubber dam and was nonresponsive to hot water. The M F canal was obturated using laterally condensed gutta-percha and Roth's 80l sealer. The access was sealed with an IRM temporary restoration and the patient was referred for permanent restoration. The patient has remained comfortable for more than a year (Fig. 4).
unprepared canal. In both o f these cases, a missed canal containing vital pulp tissue was located and removal of the remaining pulp tissue eliminated the clinical symptoms. Interestingly, in both cases it was sensitivity to heat which was responsible for the clinical symptoms of an acute pulpalgia. It may be hypothesized that the sensitivity to heat was due to a change in the intraputpal pressure. Beveridge and Brown (1) demonstrated that the application of heat caused a 45 m m Hg rise in intrapulpal pressure. When the heat was removed, the pressure returned to a level about 8 m m Hg higher than the initial pressure. They also found that the pulpal pulse pressure generally increased after the application of heat and remained higher even when the intrapulpal pressure had returned to the initial level. Cold was found to have an opposite effect, with a decrease of 28 m m Hg in intrapulpal pressure and a decrease in the pulpal pulse pressure. Heat causes vasodilation and fluid exudation with a subsequent increase in intrapulpal pressure within the limited confines of the root canal space. In the inflamed pulp, increased intrapulpal pressure already exists but at a level below pain threshold (2). The application of heat can cause a painful response which persists until the intrapulpal pressure returns to its original subthreshold level. Conversely, cold causes a vasoconstriction and contraction of fluid, resulting in a droP in intrapulpal pressure and thus there may be no pain response produced. The large metallic restoration placed in both of these teeth could have served as an excellent conductor of heat.
DISCUSSION A clinical history of thermal sensitivity in an endodontically treated tooth is strongly suggestive of vital pulp tissue in an
Journal of Endodontics
Keir et al.
In both cases, some pulp tissue maintained its vitality in spite of adequate preparation and obturation of other parts of the canal system. In the first case, the canal space had considerable calcifications noted radiographically at the initiation of treatment. The presence of these calcifications may have sufficiently isolated the facial aspect of the distal canal producing two canals and protecting the pulp tissue in that aspect of the canal from the effects of instrumentation and irrigation. The distal root of mandibular first molars has a 5 % incidence of Type IV canal anatomy (3). Also, Type V canal anatomy in the distal root can occur 8% of the time (3). This could explain why a portion of the pulp tissue in the distal canal maintained its vitality even though the lingual aspect of the canal had been instrumented and obturated. In the second case, the M F canal was missed during the original treatment. In mandibular third molars, 8.7% have three canals with the mesial root having a 13.6% incidence of Type IV canal anatomy and 65.8% incidence of Type I canal anatomy (4). This explains how the blood supply to the remaining pulp tissue in the untreated canals could have been maintained. Thus, technically, this tissue was subjected to a pulpotomy and was able to maintain its vitality despite aggressive debridement in adjacent canals.
It is easy to dismiss complaints of thermal sensitivity in previously endodontically treated teeth and to assure the patient that the source o f their problem is another tooth. As demonstrated in these two cases, this can be a mistake. Careful attention to the patient's chief complaint is of utmost importance. The key to diagnosis in both cases was reproduction of the patient's chief complaint with thermal stimulation. Dr. Keir is a resident, Department of Endodontics, Wilford Hall USAF Medical Center, Lackland AFB, TX. Dr. Walker is chairman, Department of Endedontics, Wilford Hall USAF Medical Center. Dr. Schindler is assistant chairman, Department of Endodontics, Wilford Hall USAF Medical Center. Dr. Dazey is chief, Endodontics, 22nd Strategic Hospital, March AFB, CA.
References 1. Beveridge EE, Brown AC. The measurement of human dental intrapulpal pressure and its response to clinical variables. Oral Surg 1965;19:655-58. 2. van Hassel HJ. Physiology of the human dental pulp. Oral Surg 1971 ;32:126-34. 3. Vertucci FJ. Root canal anatomy of the human permanent teeth. Oral Surg 1984;58:589-99. 4. Pineda F, Kuttler Y. Mesiodistal and buccolingual roentgenographic investigation of 7,275 root canals. Oral Surg 1972;33:101-10.