Endodontic Pain Management: Preoperative, Perioperative, and Postoperative Strategies
Brooke Blicher, DMD; and Rebekah Lucier Pryles, DMD
Orofacial pain is often the impetus for patients to seek dental care, and endodontic disease accounts for a significant proportion of this pain. That said, fear of pain during dental procedures is a major deterrent for many prospective dental patients. Thankfully, pain management strategies have significantly improved over time. Managing endodontic pain at all stages of diagnosis and treatment-preoperative, perioperative, and postoperative-may be achieved with a variety of evidence-based and reliable pain management approaches.
The foundation of pain management is the determination of pain source and development of a definitive diagnosis. Delivery of definitive care, either by endodontic therapy or extraction, is the best way to provide complete relief of pain of endodontic origin.1 Beyond this, pain management should be considered prior to the provision of definitive care, perioperatively while care is being delivered, and postoperatively until signs and symptoms of inflammation and infection resolve. This article highlights evidence-based pain management strategies and briefly discusses the future direction of orofacial pain management.
Preoperative Pain Management
When definitive care cannot be delivered immediately, oral analgesics offer convenient and effective means to relieve even severe dental pain. Over-the-counter oral analgesics include both nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen. Ibuprofen is the most studied drug in the NSAID class due to its convenient dosing, high safety profile, and ready availability without a prescription. It functions by blocking the cyclooxygenase (COX) 1 and 2 enzymes to prevent production of prostaglandins involved in both pain transmission and inflammation.1 The maximum recommended dosage of ibuprofen is 3200 mg/day, with common dosages ranging from 400 mg to 800 mg every 4 to 8 hours.2 Major side-effects include gastrointestinal upset and are dose dependent; thus, the lowest effective dosage should be utilized.3
Furthermore, care must be exercised when prescribing NSAIDs to patients with cardiac disease. A 30% increased risk of myocardial infarction is associated with exposure to ibuprofen in the 30 days prior to the event.4 These risks exist even in patients who have taken ibuprofen for relatively short durations, particularly with dosages larger than 1200 mg/day.5 However, when compared to selective COX-2 inhibitors like celecoxib, NSAIDs, including ibuprofen, showed a lesser risk of cardiovascular disease6; thus, they remain the drug of choice, especially in patients with other cardiovascular risk factors.
Acetaminophen functions to block prostaglandin synthesis peripherally and interacts with cannabinoid and serotonergic receptors centrally.7 The manufacturer's maximum recommended dosage of acetaminophen is 3000 mg/day. Given the risk of hepatoxicity associated with acetaminophen, the lowest effective dosage is recommended.8
Prescription oral analgesics include corticosteroids and opioid class drugs. Although they have shown efficacy in treating severe dental pain, corticosteroids like prednisalone and dexamethasone have a higher side-effect profile than NSAIDs and generally have cross-reactivity when patients are sensitive to these drugs.9 Therefore, their use is not routinely recommended. Opioid class drugs include complexes of codeine, hydrocodone, oxycodone, and tramadol. These drugs act centrally on mu and kappa receptors to alter pain perception.1 Though not as effective as the pain relievers discussed above, these drugs produce feelings of euphoria and reduce anxiety; thus, patients in severe pain can rest and oftentimes escape notice of their severe pain. Nonetheless, risks of misuse and addiction, and resultant rules and regulations limiting their use, suggest avoidance of these medications whenever possible.
According to the Oxford league table, NSAIDs possess greater efficacy than opioids in the treatment of severe dental pain.10 Combination therapy utilizing NSAIDs and acetaminophen has shown greater efficacy in the treatment of severe dental pain than either drug alone.11 Mild to moderate pain is often relieved by 400 mg ibuprofen combined with 325 mg acetaminophen dosed every 6 hours, whereas more severe pain may require 600 mg or 800 mg ibuprofen and up to 1000 mg acetaminophen every 8 hours. Simultaneous administration of ibuprofen and acetaminophen has shown improved efficacy over alternating courses12 and should be encouraged.
Local anesthetics, like oral pain medications, can provide hours of pain relief for patients with endodontic pathology, particularly when longer-acting drugs like bupivacaine are utilized. Moreover, the administration of local anesthetics may further act to support a correct diagnosis when used as part of selective anesthesia.13
While oral pain medications and local anesthetics possess significant utility in managing preoperative pain, antibiotics are not effective pain relievers.14 Providers should limit their prescription to situations with uncontrolled, systemic spread of infection, or where medical compromise warrants their use prophylactically.15
Perioperative Pain Management
Perioperative pain management in endodontics centers around the achievement of profound local anesthesia. Unfortunately, patients suffering from severe pain of endodontic origin, particularly symptomatic irreversible pulpitis, may experience difficulties in achieving adequate pulpal anesthesia due to issues with techniques, altered pH, or inflammation of the surrounding tissues resulting in pharmacologic failure.1 Since neither patients nor providers wish to experience breakthrough pain during treatment, and poor past experiences can lead patients to avoid dental care in the future, it is imperative that clinicians provide pain-free care.
The literature supports specific techniques for achieving pulpal anesthesia in teeth with symptomatic irreversible pulpitis. Successful pulpal anesthesia of maxillary teeth can be obtained by infiltrations on the buccal surfaces alone. No gains in anesthesia success are obtained through the addition of a posterior superior alveolar nerve block or palatal anesthesia.16 For mandibular teeth, achievement of successful pulpal anesthesia can be more complex. Mandibular anterior teeth may be successfully anesthetized by infiltrations alone, whereas premolars are most successfully anesthetized by the combination of mental and inferior alveolar nerve blocks (IANBs).17,18 Mandibular molars require block anesthesia, usually with the addition of an adjunctive anesthetic technique. Success rates of the IANB alone are quite low and alternative block techniques, including the Gow-Gates and Vazirani-Akinosi, show no greater effectiveness.18,19 Buccal infiltration with articaine exhibits the greatest efficacy as an adjunct to the IANB block, although other techniques, including intraligamentary and intraosseous anesthesia, are also effective.20 When all else fails, or when breakthrough sensitivity occurs mid-procedure, intrapulpal anesthesia may be used.21
In general, the type of anesthetic solution selected does not appear to impact anesthetic success. Both articaine and lidocaine provide equally efficacious infiltration anesthesia.22 When considering block anesthesia, no differences have been found in the efficacy of commonly available mepivacaine and lidocaine solutions.23 Articaine and other 4% solutions are discouraged for block anesthesia due to increased risks of paresthesia.24
Adequate dosages of any of these drugs must be used to achieve profound pulpal anesthesia, as a dose-response relationship exists. Administration of 3.6 mL of anesthetic solution via IANB shows significantly fewer pulpal anesthesia failures in mandibular molars than 1.8 mL of solution.25
Local anesthesia alone may be insufficient for perioperative pain control in some patients. In such cases, additional pharmacologic agents may be used to increase its efficacy. Nitrous oxide itself acts as an analgesic and can improve the efficacy of local anesthetic solutions. Benzodiazepines, however, do not potentiate the effects of local anesthetics, and should only be expected to reduce procedure-related patient anxiety. Preoperative use of oral analgesics, including dexamethasone, NSAIDs, and tramadol, may improve effectiveness of IANB injections in patients with symptomatic irreversible pulpitis, although controversy exists.26-28
Postoperative Pain Management
While definitive treatment of endodontic pathology is the optimal means to alleviate severe pain, some degree of postoperative discomfort is normal. Most patients report mild discomfort after endodontic treatment with minimal impact on daily living. Only 6% of patients report more acute pain following treatment, consistent with a postoperative flare-up. Patients report resolution of most pain symptoms within 2 to 3 days, and 90% report complete pain relief by 1 week following endodontic treatment.29 Since postoperative pain is common and to be expected, clinicians need to warn patients to anticipate its presence and arm them with strategies to minimize its impact. In addition to verbal communication, written instructions can effectively help manage patient expectations and clearly define normal and abnormal conditions that may warrant contacting an available emergency provider.
Like in the management of preoperative pain, oral medications, including combination therapy with ibuprofen and acetaminophen, are most appropriate for the management of postoperative pain. Opioid class drugs are less effective and should be avoided if possible. Long-acting anesthetics like bupivacaine are useful adjuncts to ensure pain relief through the acute postoperative period when pain can be most severe. Bupivacaine possesses properties to provide extended analgesia even beyond its half-life, according to studies in the medical literature.30
Future Considerations
Areas of development to further improve profound pulpal anesthesia include a promising nasal spray that can anesthetize the maxillary anterior sextant.18 Also, given the significance of opioid misuse, research will no doubt focus on the development of non-addictive alternative substances. Newer formulations of existing drugs may increase their bioavailability and potency.
About the Author
Brooke Blicher, DMD
Clinical Instructor, Department of Restorative Dentistry and Biomaterials Sciences, Harvard School of Dental Medicine, Boston, Massachussetts; Assistant Clinical Professor, Department of Endodontics, Tufts University School of Dental Medicine, Boston, Massachusetts; Diplomate, American Board of Endodontics; Private Practice limited to Endodontics, White River Junction, Vermont
Rebekah Lucier Pryles, DMD
Assistant Clinical Professor, Department of Endodontics, Tufts University School of Dental Medicine, Boston, Massachusetts; Lecturer, Department of Restorative Dentistry and Biomaterials Sciences, Harvard School of Dental Medicine, Boston, Massachusetts; Diplomate, American Board of Endodontics; Private Practice limited to Endodontics, White River Junction, Vermont
References
1. Keiser K, Hargreaves KM. Building effective strategies for the management of endodontic pain. Endod Topics. 2002;3:93-105.
2. Gage TW, Pickett FA. Mosby's Dental Drug Reference. 7th ed. St Louis MO: Mosby; 2005
3. Hargreaves KM, Troullos ES, Dionne RA. Pharmacologic rationale for the treatment of acute pain. Dent Clin North Am. 1987;31(4):675-694.
4. Sondergaard KB, Gislason G. NSAIDs and cardiac arrest: non-steroidal anti-inflammatory drug use is associated with increased risk of out-of-hospital cardiac arrest: a nationwide case-time-control study. Eur Heart J. 2017;38(23):1788-1789.
5. Bally M, Dendukuri N, Rich B, et al. Risk of acute myocardial infarction with NSAIDs in real world use: Bayesian meta-analysis of individual patient data. BMJ. 2017;357:j1909.
6. Barcella CA, Lamberts M, McGettigan P, et al. Differences in cardiovascular safety with non-steroidal anti-inflammatory drug therapy - a nationwide study in patients with osteoarthritis. Basic Clin Pharmacol Toxicol. 2019;124(5):629-641.
7. Yagiela JA, Neidle EA, Dowd FJ. Pharmacology and Therapeutics for Dentistry. St. Louis, MO: Mosby; 1998.
8. James LP, Mayeux PR, Hinson JA. Acetaminophen-induced hepatotoxicity. Drug Metab Dispos. 2003;31(12):1499-1506.
9. Shamszadeh S, Shirvani A, Eghbal MJ, Asgary S. Efficacy of corticosteroids on postoperative endodontic pain: a systematic review and meta-analysis. J Endod. 2018;44(7):1057-1065.
10. Richards D. The Oxford Pain Group League table of analgesic efficacy. Evid Based Dent. 2004;5:22-23.
11. Menhinick KA, Gutmann JL, Regan JD, et al. The efficacy of pain control following nonsurgical root canal treatment using ibuprofen or a combination of ibuprofen and acetaminophen in a randomized, double-blind, placebo-controlled study. Int Endod J. 2004;37(8):531-541.
12. Derry CJ, Derry S, Moore RA. Single dose oral ibuprofen plus paracetamol (acetaminophen) for acute postoperative pain. Cochrane Database Syst Rev. 2013;(6):CD010210.
13. Berman LH, Hartwell GR. Diagnosis. In: Hargreaves KM, Cohen S, Berman LH, eds. Cohen's Pathways of the Pulp. St Louis, MO: Mosby; 2011:2-39.
14. Aminoshariae A, Kulild JC. Evidence-based recommendations for antibiotic usage to treat endodontic infections and pain: a systematic review of randomized controlled trials. J Am Dent Assoc. 2016;147(3):186-191.
15. AAE position statement. AAE guidance on the use of systemic antibiotics in endodontics. J Endod. 2017;43(9):1409-1413.
16. Aggarwal V, Singla M, Miglani S, et al. A prospective, randomized, single-blind comparative evaluation of anesthetic efficacy of posterior superior alveolar nerve blocks, buccal infiltrations, and buccal plus palatal infiltrations in patients with irreversible pulpitis. J Endod. 2011;37(11):1491-1494.
