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CONSORT Randomized Clinical Trial

Comparative Evaluation of Effect of Preoperative Oral Medication of Ibuprofen and Ketorolac on Anesthetic Efcacy of Inferior Alveolar Nerve Block with Lidocaine in Patients with Irreversible Pulpitis: A Prospective, Double-blind, Randomized Clinical Trial
Vivek Aggarwal, MDS,* Mamta Singla, MDS, and Debipada Kabi, MDS*
Abstract
Introduction: Anesthetic efcacy of inferior alveolar nerve block decreases in patients with irreversible pulpitis. It was hypothesized that premedication with nonsteroidal anti-inammatory drugs might improve the success rates in patients with inamed pulps. Methods: Sixty-nine adult volunteers who were actively experiencing pain participated in this prospective, randomized, double-blind study. The patients were divided into 3 groups on a random basis and were randomly given 1 of the 3 drugs including ibuprofen, ketorolac, and placebo 1 hour before anesthesia. All patients received standard inferior alveolar nerve block of 2% lidocaine with 1:200,000 epinephrine. Endodontic access preparation was initiated after 15 minutes of initial inferior alveolar nerve block. Pain during treatment was recorded by using a Heft Parker visual analog scale. Success was recorded as none or mild pain. Results: Statistical analysis with nonparametric c2 tests showed that placebo gave 29% success rate. Premedication with ibuprofen gave 27%, and premedication with ketorolac gave 39% success rate. There was no signicant difference between the 3 groups. Conclusions: Preoperative administration of ibuprofen or ketorolac has no signicant effect on success rate of inferior alveolar nerve block in patients with irreversible pulpitis. (J Endod 2010;36:375378)

Key Words
Ibuprofen, inferior alveolar nerve block, irreversible pulpitis, ketorolac, NSAIDs

From the *Department of Dental Surgery, Safdarjung Hospital, New Delhi; and Department of Conservative Dentistry and Endodontics, Institute of Dental Sciences and Technology, Modinagar, India. Address requests for reprints to Dr Vivek Aggarwal, Department of Dental Surgery, Safdarjung Hospital, New Delhi, India. E-mail address: drvivekaggarwal@gmail.com. 0099-2399/$0 - see front matter Copyright 2010 American Association of Endodontists. doi:10.1016/j.joen.2009.11.010

ocal anesthesia is an integral part of management of painful endodontic emergencies by inhibiting the nociceptive signals (14). The inferior alveolar nerve block (IANB) is the standard and most commonly used technique for achieving pulpal anesthesia for mandibular endodontic procedures. IANB has a high failure rate, ranging from 7% 77% (2, 3, 510). The success rates get even worse in patients with inamed pulpal tissues (2, 3, 10, 11). Various mechanisms have been hypothesized to explain the failure of local anesthetics including anatomic variations like cross innervations and accessory innervations (1114), decreased local pH (2, 14), tachyphylaxis of anesthetic solutions (14), and activation of nociceptors including tetrodotoxin (TTX) and capsaicin-sensitive transient receptor potential vanilloid type 1 (TRPV1) (1416). The most plausible explanation for decrease in success rate in inamed pulp can be the activation of nociceptors by inammation (1517). Inammatory mediators reduce the threshold for activation of nociceptor neurons to a point that a minor stimulus now might re these neurons (17, 18). This inammatory process is mediated via prostaglandins (PGs), which are end products of arachidonic acid (AA) metabolism, produced via cyclooxygenase (COX) pathway (19, 20). PGs act by sensitizing nerve endings to bradykinins and histamines and hence enhance the pain and tenderness of inammation (1520). COX is available in body in 2 isoforms, COX-1 and COX-2 (21, 22). COX-1 regulates normal cell activities in the stomach, kidneys, and platelets by synthesizing prostanoids that have cytoprotective functions (21, 22). The COX-2 is normally not present in tissue (except kidneys) and is present only in areas of tissue injury and inammation (22, 23). Traditional nonsteroidal anti-inammatory drugs (NSAIDs) act by nonselective inhibition of COX activity, resulting in some gastrointestinal side effects (23). Specic COX-2 inhibitors were developed to deliver equivalent pain relief to that of the nonselective NSAIDs, but without the accompanying risk of gastrointestinal complications. Recently a number of large clinical trials have revealed that the COX-2specic inhibitors are associated with an increased risk of cardiovascular toxicity, which led to withdrawal of Rofecoxib from the market in 2004 (2427). Among the nonselective NSAIDs, ibuprofen and ketorolac have been shown to provide signicantly improved pain control over placebo (2830). Ibuprofen is a propionic acid derivative and an effective analgesic and anti-inammatory agent. Ketorolac, a pyrrolo-pyrrole derivative, is as effective as morphine or meperidine for pain relief (2831). Many researchers have identied inammation as an important component of the pathogenesis of hyperalgesia and failure of local anesthesia (1520). Because NSAIDs reduce nociceptor activation by decreasing the levels of inammatory mediators, it is hypothesized that premedication with NSAIDs will affect the success rate of local anesthesia in patients with irreversible pulpitis. In 2007 Modaresi et al (32) studied the role of premedication with ibuprofen and acetaminophen-codeine for achieving deep anesthesia in patients with irreversible pulpitis. Efcacy in achieving deep anesthesia was evaluated with the help of electric pulp tester. The authors did not evaluate the success or failure rate on basis of pain during root canal treatment. Therefore the present study

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TABLE 1. Comparison of Age, Gender, Initial and Postinjection Pain Control PLAC
Age (y) Gender Initial pain (Heft Parker VAS) Postinjection pain (after 15 min)
PLAC, placebo; IBUP, ibuprofen; KETA, ketorolac. There was no signicant difference (P > .05) between the groups.

IBUP
30 8; range, 2338 10 males, 12 females 106 38 10 4

KETA
29 8; range, 2437 12 males, 11 females 101 45 93

26 9; range, 2135 14 males, 10 females 97 44 65

was planned to evaluate the effect of premedication with various NSAIDs on anesthetic success rate in terms of pain during endodontic procedure. The purpose of this prospective, randomized, double-blind study was to compare the effect of oral premedication of ibuprofen, ketorolac, and a placebo medication on anesthetic efcacy of IANB with lidocaine with 1:200,000 epinephrine in patients with irreversible pulpitis.

Materials and Methods


Seventy-two adult volunteer subjects, who reported in the dental emergency department, participated in this 3-month-long prospective, randomized, double-blind study. The sample size calculation consisted of a level type I error of 0.05 and b level type II error of 0.20. A power calculation dictated that a sample size of 63 subjects would give 80% power to detect a 20% difference in the success rate of 2 test groups. We assumed a dropout rate of approximately 10% and enrolled at least 23 subjects in each group. The subjects were actively experiencing pain and were in good health, and none were taking any medication that would alter pain perception, as determined by oral questioning and written questionnaire. An ethical clearance was sought from the institute review committee, and an informed written consent was obtained from each subject. Preoperative radiographs were obtained. The inclusion criteria for the study were active pain in a mandibular molar; prolonged response to cold testing with an ice stick and an electric pulp tester (Kerr, Analytic Technology Corp, Redmond, WA); absence of any periapical radiolucency on radiographs, except for a widened periodontal ligament and a vital coronal pulp on access opening; and ability to understand the use of pain scales. Exclusion criteria included known allergy, sensitivity, or contraindications to any opioid or nonopioid analgesic including aspirin or NSAIDs, history of active peptic ulcer within the preceding 12 months, history of bleeding problems or anticoagulant use within the last month, patients who were pregnant or breast-feeding, a history of known or suspected drug abuse, and patients who had taken NSAIDs within 12 hours before administration of the study drugs. Patients having active pain in more than 1 mandibular molar were excluded from the study. The methodology was similar to our previous study (10). First author (V.A.) screened and recruited the patients in the study. Randomization of patients was done by simple random sampling with a linear congruential generator. Randomized allocation of the patients was done by a trained dental hygienist who was blinded to the treatment procedures. Before initiating the treatment, the patients were asked to rate their pain on a Heft Parker visual analog scale (VAS). Heft Parker VAS with
TABLE 2. Distribution of Teeth for Control PLAC, IBUP and KETA Groups Tooth
First molar Second molar

170-mm line marked with various terms describing the levels of pain was used for this purpose (33). The millimeter marks were removed from the scale, and the scale was divided into 4 categories: no pain corresponded to 0 mm; faint, weak, or mild pain corresponded to 054 mm; moderate pain corresponded to 55114 mm; and strong, intense, and maximum possible pain corresponded to more than 114 mm (3). A trained dental hygienist divided 144 empty capsules of same color and size into 3 bottles: ibuprofen (IBUP), ketorolac (KETA), and placebo (PLAC) group. IBUP capsules were lled with 300 mg of ibuprofen, KETA capsules were lled with 10 mg of ketorolac, and PLAC capsules were lled with starch. The bottles were masked with an opaque label and were randomly assigned a 3-digit alphanumeric value. Another trained dental hygienist randomly divided all the patients into 3 groups of 24 patients each and gave 2 capsules 1 hour before the procedure. Only the alphanumeric values were recorded on the data sheets to blind the experiment. After 1 hour of oral administration of the capsules, all patients received standard IANB injections by using 1.8 mL of 2% lidocaine with 1:200,000 epinephrine (Xylocaine; AstraZeneca Pharmaceutical Products, Wilmington, DE). The solution was injected by the same clinician (rst author) by using self-aspirating syringes (Septodont, SaintMaur-des-Fosses Cedex, France) and 27-gauge long needles (Septoject; Septodont). After reaching the target area, aspiration was performed, and 1.7 mL of solution was deposited at a rate of 1 mL/min. After 15 minutes of the initial IANB, each patient was asked if his or her lip was numb. If profound lip numbness was not recorded within 15 minutes, the block was considered unsuccessful, and the patients were excluded from the study. The patients were again asked to rate their pain on Heft Parker VAS. The involved teeth were isolated with a rubber dam, and a conventional access opening was initiated. Patients were instructed to raise their hand if any pain was felt during the procedure. In case of pain during the treatment, the procedure was stopped, and patients were asked to rate the pain on Heft Parker VAS. The extent of access preparation and/or instrumentation was recorded as within dentin, within pulpal space, and instrumentation of canals. Success was dened as no pain or weak/mild pain during endodontic access preparation and instrumentation (3). The ndings were recorded on a Microsoft Excel sheet (Microsoft Ofce Excel 2003; Microsoft Corp, Redmond, WA) for statistical evaluation by using the program BioEstat, version 4.0 (Mamiraua Institute, Belem, Brazil). Age and initial and postinjection pains of the subjects
TABLE 3. Comparison of Percentage of Successful Anesthesia in Control and Test Groups Control PLAC
Successful anesthesia 7 of 24 patients (29%)

IBUP
6 of 22 patients (27%)

KETA
9 of 23 patients (39%)

Control PLAC
12/24 (50%) 12/24 (50%)

IBUP
10/22 (45%) 12/22 (55%)

KETA
11/23 (48%) 12/23 (52%)

PLAC, placebo; IBUP, ibuprofen; KETA, ketorolac. There was no signicant difference (P > .05) between the groups.

PLAC, placebo; IBUP, ibuprofen; KETA, ketorolac. There was no signicant difference (P > .05) between the groups.

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were summarized by using means and standard deviations. Multiple comparison analysis of variance and post hoc tests were used to determine signicant differences at P <.05. Anesthetic success of the IBUP, KETA, and PLAC groups was dichotomous in nature and was analyzed by using c2 tests. Pathogenesis of irreversible pulpitis includes inammation of pulp, leading to breakdown of damaged cell membranes and release of AA, mediated by either secretory (sPLA2) or cytoplasmic (cPLA2) phospholipases (21, 22, 34). In response to various inammatory stimuli, AA is acted on by COX or prostaglandin H synthase (PGHS) enzymes and gets converted into 20 carbon chain molecules called eicosanoids, which are further converted by various cell-specic isomerases and synthases to produce 5 biologically active primary PGs that include PGD2, PGE2, PGF2a, prostacyclin (PGI2), and thromboxane A2 (TxA2) (3437). PGs sensitize nerve endings to bradykinins and histamines and enhance the pain and tenderness of inammation. In the early 1990s, an inducible isoform of COX enzyme, now called COX-2, was discovered (21, 22). It is now well-accepted that COX enzymes are present in 2 isoforms: COX-1 and COX-2. The COX1 isoform is constitutively expressed at high levels in cells and tissues and is responsible for synthesizing prostanoids that have cytoprotective functions (22, 3538). The COX-1 enzymes regulate normal cell activities in endothelium, monocytes, platelets, renal collecting tubules, and seminal vesicles. The COX-2 isoform, normally not present in tissue, is induced by mediators of inammation such as lipopolysaccharides, interleukin-1, and tumor necrosis factor-alpha (22, 3537). COX enzymes consist of a COX active site and a long hydrophobic channel. The entrance of the COX channel is guarded by a network of hydrogen bonds comprising Arg120, Glu524, Tyr355, and His90 (38, 39). The carboxyl moiety of NSAIDs generally binds at Tyr385 and Arg120 and inhibits both isoforms of COX. The COX-2 (394 A) active site is 20% larger than COX-1 (316 A) (39). Hence, selective COX-2 inhibitors bind to COX-2 as a result of reduced steric and ionic crowding at the mouth of the channel (binding site) by Arg120 (3841). Because of efcacy of NSAIDs to effectively block the COX pathway, it was hypothesized that premedication with NSAIDs will help in management of patients with irreversible pulpitis by inhibiting the formation of PGs and thus minimizing the activation of nociceptors. In 2007 Modaresi et al (32) advocated premedication with ibuprofen for achieving deep anesthesia in patients with irreversible pulpitis. They evaluated the depth of anesthesia with the help of electric pulp tester and did not evaluate the success or failure rate on basis of pain during root canal treatment (32). In the present study, effect of premedication with ibuprofen and ketorolac was studied by using pain response on modied Heft Parker VAS in a prospective, randomized, double-blind trial. Success was considered as no pain or weak/mild pain during endodontic access preparation and instrumentation. Premedication was given 1 hour before the procedure to allow NSAIDs to achieve satisfactory plasma concentration. In the present study, PLAC group gave 29% success rate, which is comparable with previous studies (3, 10, 14). Premedication with ibuprofen (27%) or ketorolac (39%) did not signicantly increase the success rate. The results do not match with the ndings of Modaresi et al, although the method of evaluation is different. All the patients in the present study had active pain during the presentation. It is possible that because of acute inammatory reaction, the inammatory mediators had already activated the nociceptors. Medication with NSAIDs only inhibits the formation of PGs but has no effect on already activated nociceptors. There was no signicant difference between the pain and discomfort ratings of the patients with unsuccessful anesthesia (Heft Parker VAS score >54, moderate or strong, intense pain) with relation to extent of access preparation and/or instrumentation. Majority of the unsuccessful patients had pain during dentin penetration and did not allow penetration of the pulpal chamber. Intrapulpal anesthesia, which is a last resort in such patients, could be given only after small penetration in the pulpal 377

Results
Seventy-two adult volunteer subjects, 38 men and 34 women, with an average age of 31 years, range 2138 years, participated in this prospective, randomized, double-blind study. Of the original 72 patients, 3 patients, 2 from IBUP group and 1 from KETA group, did not have profound lip numbness at 15 minutes and were excluded from the study. The age, gender, and initial and 15-minute postinjection pain of all the patients are presented in Table 1. Distribution of teeth for PLAC (control), IBUP, and KETA groups is presented in Table 2. There was no statistical difference between the age (P = .72), gender (P = .94), initial pain (P > .05), and distribution of teeth. All patients included in the study had profound lip anesthesia after 15 minutes. All patients reported a signicant decrease in active pain after local anesthesia (P < .05). The postinjection pain Heft Parker VAS scores of different groups were insignicant (P = .94). The comparison of percentage of patients with successful anesthesia (no pain or weak/mild pain during endodontic access preparation and instrumentation) is presented in Table 3. Control PLAC gave 29% success rate (7 of 24 patients). Premedication with ibuprofen (IBUP) gave 27% (6 of 22 patients), and premedication with ketorolac (KETA) gave 39% (9 of 23 patients) success rate. There was no significant difference between the 3 groups. None of the techniques gave 100% success rate. The pain and discomfort ratings of the patients with unsuccessful anesthesia (Heft Parker VAS score >54) with relation to extent of access preparation and/or instrumentation are presented in Table 4.

Discussion
IANB is an effective tool in management of mandibular endodontic procedures by reversibly interrupting the propagation of inferior alveolar nerve impulses. IANB might provide successful anesthesia in 70% of uninamed pulp, but the success rate drastically decreases to 30% or even less in patients with irreversible pulpitis (2, 3, 510). The literature suggests activation of nociceptors by inammatory mediators such as PGs as a major cause of increased incidence of failure of IANB in patients with irreversible pulpitis (1520).
TABLE 4. Comparison of Number of Unsuccessful Anesthesia in Control and Test Groups Heft Parker VAS score 54114
Within dentin Within pulpal space Instrumentation of canals Control PLAC IBUP KETA Control PLAC IBUP KETA Control PLAC IBUP KETA 5 of 17 4 of 16 4 of 14 2 of 17 2 of 16 3 of 14 2 of 17 2 of 16 2 of 14

Heft Parker VAS score >114


3 of 17 5 of 16 3 of 14 4 of 17 3 of 16 1 of 14 1 of 17 2 of 16 1 of 14

VAS, visual analog scale.

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roof. In the present study, intraosseous injection was used in further management of patients with unsuccessful anesthesia. It should also be noted that although all the patients had subjective symptoms of lip numbness, the anesthesia was not successful in all cases. This phenomenon is also seen in uninamed pulps, in which in spite of successful lip numbness, the clinician failed to get a response to the maximum stimulus on electric pulp testing (811, 14). A further clinical study on a larger sample size, with the latest NSAIDs, is planned to strengthen the results. In conclusion, preoperative administration of ibuprofen or ketorolac has no signicant effect on success rate of IANB in patients with irreversible pulpitis. There was no signicant difference between the ibuprofen or ketorolac groups.
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Supplementary data
Supplementary data associated with this article can be found, in the online version, at doi:10.1016/j.joen.2009.11.010

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