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Pain Control

By Paul A. Rosenberg, D.D.S.

Endodontic pain is multifaceted. Its consideration is critical for clinicians and their patients. In the past, pain was considered synonymous with Endodontic treatment. This is no longer true, as treatment can now be predictably provided without significant intra or post-operative pain. Complete discussion of the subject would include topics ranging from immunologic and inflammatory reactions, predisposing factors including the influence of genetics and gender as well as psycho-social factors. This communication will illuminate specific areas of importance to clinicians as they implement evidence-based strategies to prevent and/or treat pain.

Incidence of Flare-ups

A classic review noted that reported incidence of flare-ups ranges from 1.4%-19%. (1) This wide range of estimates can be disconcerting and is the result of different research methodologies, varied inclusion and exclusion criteria, differences in sample size and statistical analysis. Those variations also explain why clinical studies concerning Endodontic pain may reach different conclusions. Readers are advised to review more than one evidence-based report before reaching conclusions concerning the merits of a particular strategy.

Predicting Pain

An analysis of 374 single-visit cases determined that the incidence of post-endodontic pain was significantly lower when the treated tooth was not a molar (P=0.003), demonstrated periapical radiolucencies (P= 0.003), had no history of previous pain or emergency endodontic treatment (P=0.045) and had no occlusal contact (P=0.0001). The probability of experiencing moderate or severe pain was higher in mandibular teeth (P=0.045) and decreased in males (P=0.007). (2) Another study of 652 patients, using a different methodology, determined that pretreatment pain is an important predictor of postoperative pain. A diagnosis of symptomatic apical periodontitis was also a predictor of severe postoperative pain and pain was made worse by stress. (3) These findings can be valuable tools for patient education during discussions prior to treatment. There are other factors, some of which are less visible, that may also be predispose patients to pain. For example, there is increasing evidence that genetic factors, previous chronic pain conditions and the patient’s level of anxiety and gender may play a role in patients’ experience of postoperative pain. (4)


Profound local anesthesia is of prime importance in a pain prevention strategy. It needs to be emphasized that a “numb lip” is insufficient evidence of profound local anesthesia and may only indicate soft tissue anesthesia. A clinical study determined that soft tissue signs are inadequate during root canal therapy. Patients who received a negative response to a cold test, following a numb lip, were approximately 80% less likely to experience pain during endodontic treatment compared to subjects with soft tissue signs of anesthesia alone. (5)

Local anesthesia is particularly challenging for mandibular molars diagnosed with symptomatic irreversible pulpitis. A single inferior alveolar nerve block is usually inadequate to provide complete local anesthesia for mandibular molars diagnosed with symptomatic irreversible pulpitis. The clinician is advised to develop skills using supplemental anesthetic techniques including ligamental, intra-osseous and intra-pulpal. Appropriate utilization of these alternative approaches can completely change the course of what otherwise would be an extraordinarily painful experience. An excellent review of local anesthesia is available in a text titled, “Successful Local Anesthesia for Restorative Dentistry and Endodontics”, Second Edition. (6)

Exacerbation of pain in teeth with vital pulps is often iatrogenic in nature and associated with specific clinical errors. Inaccurate measurement control or failure to maintain an accurate measurement often result in pericementitis and pain. Similarly, obturating canals while the tooth remains symptomatic often causes increased and prolonged post-operative discomfort. Biologically, the challenge in treating a vital tooth is to avoid further trauma to inflamed, richly innervated pulpal and periapical tissues. Occlusal reduction is an evidence-based pain preventive strategy. A statistically valid profile was developed of patients most likely to benefit from occlusal reduction, over a 48-hour period, following canal instrumentation. Occlusal reduction should prevent postoperative pain in those patients whose teeth initially exhibit pulp vitality, percussion sensitivity, preoperative pain, and/or the absence of a periradicular radiolucency. (P=0.05). (7)

A recent randomized controlled study evaluated post-treatment endodontic pain following occlusal reduction of mandibular teeth diagnosed with symptomatic irreversible pulpitis and sensitivity to percussion. Occlusal reduction lowered the risk of moderate to severe pain by about 40%, 12 hours post-instrumentation and the overall risk of pain by 25%, 24 hours post-instrumentation. (8) Exacerbation of non- vital (necrotic) teeth during treatment is the result of bacteria and their by-products passing through periapical foramina into the surrounding tissues. When this increased bacterial load overwhelms host defenses the result can be severe pain with or without swelling. Prevention depends upon keeping instrumentation, irrigation and obturation within the canal space. In addition, simply opening into a necrotic pulp can have a profound affect as an essentially anaerobic environment is modified and the bacterial flora changes.


Treatment of an exacerbation may have clinical and pharmacologic components and is dependent on determining the cause of the problem. For example, treatment of a flare-up with symptomatic irreversible pulpitis following instrumentation depends on the clinician’s assessment of the cause. Was the measurement accurate and maintained? Was the pulp fully extirpated? Is there an additional canal? If indicated, was the occlusion reduced? Understanding the cause leads to a determination of the appropriate treatment. If the cause has been determined to be over-instrumentation, through the apex of the tooth, analgesics become essential.

In recent years, there has been a shift away from the routine use of opioids as the analgesics of choice because of their inherent potential for abuse. Increasingly, based on the best available evidence, combinations of ibuprofen and acetaminophen have replaced opioids as the analgesics of choice. Interestingly, a study could find no references in the literature in which investigators found acetaminophen-hydrocodone combinations, as currently prescribed and formulated, to be more effective than non-steroidal anti-inflammatory drugs (NSAIDS). (9) A randomized, five-parallel-group-placebo controlled trial comparing efficacy and tolerability of analgesic combination including a novel single–tablet combination of ibuprofen/paracetamol for post-operative dental pain, determined that peak pain relief was higher and sustained longer with the combination of ibuprofen/acetaminophen than ibuprofen/codeine or acetaminophen/codeine formulations. (10) The clinician’s anticipation of a patient’s pain is a signal to implement a preventive strategy. When analgesics are required, it is important not to wait for the onset of pain to initiate the therapy.

Exacerbations of non-vital teeth during treatment are the result of bacteria and their by-products passing through the periapical foramina into the surrounding tissues. When this increased bacterial load overwhelms host defenses the result can be severe pain with or without swelling. Treatment of endodontic exacerbations associated with non-vital pulps is directed at the root canal space. Re-instrumentation and copious irrigation with sodium hypochlorite is utilized to reduce the intra-canal concentration of bacteria. As this is accomplished, the patients inflammatory and immune defense mechanisms bring the biologic process under control.

Fluctuant swellings are candidates for incision and drainage in-order to relieve pressure and remove pus from the area. Antibiotics should not be used routinely to treat an exacerbation. The reader is referred to the AAE publication, Colleagues for Excellence, for guidelines concerning the use of supplemental antibiotics. (11) Prevention of exacerbations of non-vital cases depends upon keeping instrumentation, irrigation and obturation within the canal space. Pumping instruments in a vertical direction is to be avoided as those forces can push debris into periapical tissues. However, simply opening a non-vital case alters what may have been in an anaerobic condition and results is an altered bacterial flora that can cause an exacerbation. (12)


Endodontic treatment today can be a virtually pain free experience. Evidence-based clinical and pharmacologic strategies can be integrated to avoid, minimize or treat Endodontic pain.


(1) Walton R and Fouad A. Endodontic interappointment flare-ups: a prospective study of incidence and related factors. J Endod 1992; 18: 172-77.
(2) Arias A, de la Macorra JC, Hidalgo JJ, Azabal M. Predictive models of pain following root canal treatment: a prospective clinical study. Int Endod J 2013;46:784-793 .
(3) Law AS, Nixon DR, Aguirre AM and National Dental PBRN Collaborative Group. Predicting severe pain after root canal therapy in the National Dental PBRN J Dent Res, March 2015: 94 (3 Clinical Suppl) 37 S-43 S.
(4) Kahn AA, Maixner W, PF Lim. Persistent pain after endodontic therapy. JADA 2014; 145:270-272.
(5) Hsaio -Wu, GW. Susaria SM, White RR. Use of the cold test as a measure of pulpal anesthesia during Endodontic therapy: a randomized, blinded placebo-controlled clinical trial. J Endod 2007: 33;406-410.
(6) Reader A, Nusstein J, Drum M. Successful Local Anesthesia for Restorative Dentistry and Endodontics, Second Edition, Quintessence Publishing, 2017,240 pp.
(7) Rosenberg PA, Babick PJ, Schertzer L, and Leung A. The effect of occlusal reduction on pain after endodontic instrumentation. J Endod 1998; 1:492-496.
(8) Ahmed YE, Emara RS, Sarhan SM, Boghdadi RM, et al. Post-treatment endodontic pain following occlusal reduction in mandibular posterior teeth with pulpitis and sensitivity to percussion: a single center randomized controlled trial. Int Endod J 2020;53:1170-1180.
(9 ) Moore PA, Dionne R, Cooper SA, and Hersh EV. Why so we prescribe Vicodin? JADA 2016;147:P530-533
(10) Daniels SE, Goulder MA, Aspley S, Reader s. A randomized, five-parallel-group-placebo controlled trial comparing efficacy and tolerability of analgesic combination including a novel single–tablet combination of ibuprofen/paracetamol for post-operative pain. Pain 2011; 152632-642.
(11) Johnson MD, Endodontics and Antibiotic Update, Fall 2019 Endodontics Colleagues for Excellence Newsletter
(12) Rosenberg PA. Endodontic Pain: Diagnosis, Causes, Prevention, Treatment. Springer, 2014, pp.183.

Dr. Paul Rosenberg served as Professor and Chair of the Department of Endodontics, Director of the Advanced Education Program and Director of the International Program, at New York University College of Dentistry from 1990-2012.  He was Associate Dean for Graduate Programs from 2000-2005. Dr. Rosenberg is a past Director of the American Board of Endodontics 2002-2008 and was a member of the Scientific Advisory Board of the Journal of Endodontics.  He has published extensively in journals and textbooks and has lectured nationally and internationally on Endodontic pain. His textbook titled, Endodontic Pain: Diagnosis, Causes, Prevention and Treatment, was published in 2014 by Springer. In 2000, Dr. Rosenberg won the Distinguished Teaching Award, which is the highest award for teaching at NYU.  In December 2007, NYU College of Dentistry unveiled a new facility, the Paul and Maxine Rosenberg Educational Wing in his honor, dedicated to providing post-graduate students with a facility devoted to their specific needs. Dr. Rosenberg received the I.B. Bender Lifetime Educator Award from the American Association of Endodontics in 2017.