The Root of the Pain

Dental sales reps are wise to understand the clinical strategies for pain management during all phases of endodontic treatment in order to better understand their customers’ needs.

Oral health professionals often perform endo­dontic treatment — or, in layman’s terms, root canal therapy — when their patients present with inflamed and/or infected pulpal tissue. Pretreatment histologic pulp status can have a direct correlation to a patient’s odontogenic pain symptoms. Therefore, pain management in endo­dontic treatment is an important clinical consideration for your customers. Pain, as reported by a patient before, during and/or after endodontic treatment, should be managed clinically with local anesthesia, endodontic treatment and medications — all of which you, as an authorized dealer, can supply to dental practices. This article provides an overview of pain management strategies commonly employed in endo­dontic treatment.

Pain Management


It is paramount for clinicians to obtain profound anesthesia when providing endodontic treatment. A common mistake is not objectively testing if pulpal anesthesia has been achieved prior to initiating therapy. Often, the only determination made to confirm if a patient is properly anesthetized is the subjective anesthesia level, as reported by the patient. Studies have demonstrated that, on average, inferior alveolar nerve anesthetic blocks administered to patients with mandibular teeth diagnosed with irreversible pulpitis had only a 55% incidence of profound pulpal anesthesia, even in the presence of 100% lip numbness, as reported by the patient.1,2

Therefore, prior to administering local anesthesia for endodontic treatment, clinicians should objectively assess the treatment tooth using a cold test and/or an electric pulp tester (EPT). With a preoperative baseline of the pulp sensibility level, once anesthesia is achieved, retesting the treatment tooth with cold or an EPT can assess the level of anesthesia. If the post-anesthesia test results are negative to cold or there is no response to EPT, profound pulpal anesthesia has likely been achieved. It is important to note, however, that teeth with metal restorations can provide a false positive test when using an EPT. In addition, Fuss et al3 reported that using an EPT was less reliable than cold testing in young patients.


Clinicians perform endodontic treatment to significantly reduce pretreatment odontogenic pain due to acute pulpal inflammation.4 Studies have demonstrated that pulpotomy and pulpectomy treatment will reduce preoperative tooth pain.5,6

Ricucci et al7 found that a clinical pulpal diagnosis of a normal pulp or reversible pulpitis had a 96.6% histological match to the actual pulp tissue in the teeth. Therefore, patients who present with pain from a carious pulp exposure and a pulp diagnosis of reversible pulpitis can be successfully treated with a pulpotomy and mineral trioxide aggregate (MTA) if the pulp is exposed during treatment.8 A randomized clinical trial by Hilton et al9 demonstrated that MTA, a bioceramic material,10 performed significantly better than calcium hydroxide as a direct pulp-capping agent.

endodontic thinking

In teeth with signs and symptoms suggestive of a pretreatment pulpal diagnosis of symptomatic irreversible pulpitis, pulpal conditions have less than a 15.6% chance of reverting to normal by a pulpotomy alone; thus, a pulpectomy is the treatment of choice.7 If the pretreatment pulpal diagnosis is a necrotic pulp, a pulpotomy is contraindicated, and a pulpectomy should be performed.

On posterior teeth, occlusal reduction should be performed prior to creating endodontic access. Occlusal adjustment may help reduce postoperative pain in patients who present with preoperative pain, pulp vitality, percussion sensitivity and/or the absence of a periradicular radiolucency.11


Conventional endodontic thinking is that files shape and irrigants clean. Root canal morphology is often complex, which makes it challenging to prepare canals by removing all vital or non-vital pulp tissue using endodontic files alone.12 A possible explanation for the inefficiency of file canal preparation is that nickel-titanium rotary files tend to stay centered in the canal and may not make contact with all dentinal walls.13

Clinicians employ various irrigants and medicaments when removing vital or necrotic pulp tissue from a canal. The use of sodium hypochlorite (NaOCl) as a canal irrigant can dissolve vital pulp tissue and disinfect a canal system,14 and it is especially important to use NaOCl irrigation when treating an inflamed vital pulp. It is also an effective irrigant when removing necrotic pulp tissue.

The use of ethylenediaminetetraacetic acid (EDTA) in conjunction with NaOCl helps remove inflamed or infected pulpal tissue from the canal wall. This is a chelating agent that aids in the removal of the smear layer, allowing irrigants and medicaments to kill microogranisms in dentinal tubules and small accessory canals. Available for clinical use as a 17% solution and in gel form, the solution is used as a final rinse prior to obturation. Additionally, EDTA gel should be placed on every file prior to activating it in a canal.

Calcium hydroxide and chlorhexidine intracanal medicaments can also help reduce pain after endodontic therapy. When compared to calcium hydroxide or the use of no medicaments, an in vivo study by Singh et al15 found that in patients with a diagnosis of necrotic pulp and acute apical periodontitis, the use of chlorhexidine alone or calcium hydroxide and chlorhexidine as an interappointment medicament reduced postoperative pain.

When treating necrotic pulps, Walton and Fouad16 demonstrated that the frequency of posttreatment flare-ups was significantly higher in necrotic pulp cases than vital cases. A flare-up is characterized by the development of pain and/or swelling following endodontic treatment. Although the etiology of posttreatment flare-ups encompasses mechanical, chemical and/or microbial agents, microorganisms are arguably the major causative factor.17 Yoldas et al18 reported that two-visit treatment on teeth with necrotic pulps demonstrated a significant reduction of interappointment flare-ups.


Anesthesia: Numbing action to isolate a specific area of the mouth during dental treatment; when localized, it may be referred to as local anesthesia.
Irreversible pulpitis: Occurrence of spontaneous pain or pain that lingers after the stimulus is removed.
Pulpotomy: Partial removal of the pulp, including the diseased portion.
Pulpectomy: Complete removal of the pulp.
Bioceramics: Calcium silicate-based materials that are biocompatible, nontoxic, nonshrinking and generally stable within a biological environment; form calcium hydroxide and hydroxyapatite; indicated for pulp capping, root repair and root canal obturation.
Chelating agent: Formulated to remove calcium ions.
Smear layer: Residual canal debris left on the canal walls from instrumentation.
Ethylenediaminetetraacetic acid: Abbreviated as EDTA, this gel formula has been shown to prevent dentinal chips and pulp collagen from blocking a canal to the point clinicians cannot maintain proper working length.
Hyperalgesia: Spontaneous pain, reduced pain threshold and/or increased perception to noxious stimuli.


The most consistent predictive factor for postoperative endodontic pain is the presence of preoperative hyperalgesia.19 Ali et al20 showed that postoperative pain was present in 54.5% of patients treated. A common mistake made by clinicians when managing endodontic pain is prescribing drugs posttreatment without critically assessing if they are pharmacologically treating inflammation and/or infection. Fouad et al21 found that antibiotics do not have an analgesic effect on odontogenic inflammatory pain. A clinical guide for determining inflammation and/or infection is the pretreatment endodontic and periradicular diagnosis. If the treatment diagnosis is irreversible pulpitis with or without symptomatic apical periodontitis, this is strictly inflammation and anti-inflammatory agents — nonsteroidal anti-inflammatory drugs (NSAIDs), for example — are the medication of choice.

A significant reduction in odontogenic pain from inflammation can be seen from taking 400 to 800 mg of ibuprofen.22 Tagger et al23 found that ibuprofen sodium dihydrate provided faster pain relief than ibuprofen acid. For patients with odontogenic-type inflammation, administering a combination of ibuprofen and acetaminophen can help manage pain.24 Acetaminophen alone or in combination with an opioid (e.g., hydrocodone) is a good alternative analgesic in patients who cannot take NSAIDs.6

There will be cases in which NSAIDs do not relieve a patient’s odontogenic postoperative pain. Although opioids are commonly prescribed in these scenarios, clinicians may prescribe dexamethasone, a synthetic adrenocortical steroid.25 If there is an odontogenic infection, a patient should be placed on an antibiotic, too, because steroids can block or mask the body’s response to infection.

The trend in prescribing antibiotics is as adjunctive treatment to conventional or surgical endodontic therapy. This adjunctive antibiotic treatment may be necessary to prevent the spread of infection, in acute apical abscesses with systemic involvement, and in progressive, persistent infections.26 Systemic involvement in clinical infection can appear as fever, swelling, malaise, compromised airway, cellulitis and/or a medically compromised patient.

Penicillin V potassium (Pen VK) is the antibiotic of choice for endodontic infections.27 It has been demonstrated that its spectrum of antimicrobial activity includes many of the bacteria that have been isolated in endodontic infections.28 However, amoxicillin and clavulanic acid are indicated for the treatment of immunocompromised patients who may have odontogenic infections containing nonoral bacteria.28

For patients who are allergic to penicillin/amoxicillin or if penicillin/amoxicillin has been ineffective, clindamycin is the second antibiotic of choice. It is beta-lactamase resistant (unlike Pen VK) and has a good spectrum against gram-positive and gram-negative bacteria.29 Another option for clinicians is to add metronidazole along with Pen VK, which has a narrow therapeutic spectrum against obligate anaerobic bacteria.30 However, metronidazole should not be prescribed alone, but used in combination with Pen VK.

Loading dose is another important consideration because antibiotics with long half-lives can require several days of therapy to take full effect. The most critical time for antibiotic efficacy is the first 24 hours, as this is typically when inoculum of infection is high and likely to harbor resistant subpopulations of bacteria.31,32 Antibiotic regimens in endodontic therapy should extend seven to 10 days. Although patients typically respond to antibiotic therapy within 24 to 48 hours, the full dosage should be finished to prevent a rebound effect of the active infection. Clinicians should remain in close contact with patients on antibiotics in the event clinical symptoms worsen or there is a drug allergy.33 Finally, if an endodontic patient presents with intraoral fluctuant swelling, the clinician should perform an incision-and-drain procedure.34


Appropriate pain management in endodontic therapy requires a solid understanding of local anesthesia, conventional endodontic treatment and clinical pharmacology. Equipped with this clinical knowledge, sales reps are well positioned to provide the tools and products their dentist customers will need to help manage the pain reported by their endodontic patients.




  1. Cohen HP, Cha BY, Spangberg LS. Endodontic anesthesia in mandibular molars: a clinical study. J Endod. 1993;19:370–373.
  2. Nusstein J, Reader A, Nist R, Beck M, Meyers WJ. Anesthetic efficacy of the supplemental intraosseous injection of 2% lidocaine with 1:100,000 epinephrine in irreversible pulpitis. J Endod. 1998;24:487–491.
  3. Fuss Z, Trowbridge H, Bender IB, Rickoff B, Sorin S. Assessment of reliability of electrical and thermal pulp testing agents. J Endod. 1986;12:301–305.
  4. Hargreaves KM, Keiser K. New advances in the management of endodontic pain emergencies. J Calif Dent Assoc. 2004;32:469–473.
  5. Hasselgren G, Reit C. Emergency pulpotomy: pain relieving effect with and without the use of sedative dressings. J Endod. 1989;15:254–256.
  6. Hargreaves KM. Management of pain in endodontic patients. Tex Dent J. 1997;114:27–31.
  7. Ricucci D, Loghin S, Siqueira J. Correlation between clinical and histological diagnosis. J Endod. 2014;40:1932–1939.
  8. Taha NA, Ahmad MB, Ghanim A. Assessment of mineral trioxide aggregate pulpotomy in mature permanent teeth with carious exposures. Int Endod J. 2017;50:117–125.
  9. Hilton TJ, Ferracane JL, Manci L, Northwest Practice-based Research Collaborative in Evidence- based Dentistry (NWP). Comparison of CaOH with MTA for direct pulp capping: a PBRN randomized clinical trial. J Dent Res. 2013;92(Suppl 7):16s–22s.
  10. Wang Z. Bioceramic materials in endodontics. Endod Topics. 2015;32:3–30.
  11. Rosenberg PA, Babick PJ, Schertzer L, Leung A. The effect of occlusal reduction on pain after endodontic instrumentation. J Endod. 1998;24:492–496.
  12. Yu DC, Tam A, Schilder H. Root canal anatomy illustrated by microcomputed tomography and clinical cases. Gen Dent. 2006;54:331–335.
  13. Guelzow A, Stamm O, Martus P, Kielbassa AM. Comparative study of six rotary nickel- titanium systems and hand instrumentation for root canal preparation. Int Endod J. 2005;38:743–752.
  14. Gernhardt CR, Eppendorf A, Kozlowski A, Brandt M. Toxicity of concentrated sodium hypochlorite used as an endodontic irrigant. Int Endod J. 2004;37:272–280.
  15. Singh RD, Khatter R, Bal RK, Bal CS. Intracanal medication versus placebo in reducing postoperative endodontic pain — a double-blind randomized clinical trial. Braz Dent J. 2013;24:25–29.
  16. Walton R, Fouad A. Endodontic inter-appointment flare-ups: a prospective study of incidence and related factors. J Endod. 1992;18:172–177.
  17. Siqueira JF. Microbial causes of endodontic flare-ups. Int Endod J. 2003;36:452–463.
  18. Yoldas O, Topuz A, Isai AS, Oztunc H. Postoperative pain after endodontic retreatment: single-versus two-visit treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004;98:483–487.
  19. Mattscheck DJ, Law AS, Noblett WC. Retreatment versus initial root canal treatment: factors affecting posttreatment pain. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2001;92:321–324.
  20. Ali A, Olivieri JG, Duran-Sindreu F, Abella F, Roig M, Garcia-Font M. Influence of preoperative pain intensity on postoperative pain after root canal treatment: A prospective clinical study. J Dent. 2016;45:39–42.
  21. Fouad AF, Rivera EM, Walton RE. Penicillin as a supplement in resolving the localized acute apical abscess. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996;81:590–595.
  22. Torabinejad M, Cymerman JJ, Frankson M, Lemon RR, Maggio JD, Schilder H. Effectiveness of various medications on postoperative pain following complete instrumentation. J Endod. 1994;20:345–354.
  23. Tagger T, Wu D, Khan A. A randomized clinical trial comparing 2 ibuprofen formulations in patients with acute odontogenic pain. J Endod. 2017;43:674–678.
  24. Cooper SA. The relative efficacy of ibuprofen in dental pain. Compend Contin Educ Dent. 1986;7:578,580–581.
  25. Krasner P, Jackson E. Management of posttreatment endodontic pain with oral dexamethasone: a double-blind study. Oral Surg Oral Med Oral Pathol. 1986;62:187–190.
  26. Segura-Egea JJ, Gould K, Sen BH, et al. Antibiotics in endodontics: a review. Int Endod J. December 22, 2016. Epub ahead of print.
  27. Kuriyama T, Karasawa K, Nakagawa K, Saiki Y, Yamamoto E, Nakamura S. Bacteriologic features and antimicrobial susceptibility in isolates from orofacial odontogenic infections. Oral Surg Oral Med Oral Pathol Oral Rad Endod. 2000;90:600–608.
  28. Baumgartner JC, Xia T. Antibiotic susceptibility of bacteria associated with endodontic abscesses. J Endod. 2003;29:44–47.
  29. Gilmore WC, Jacobus NV, Gorbach SL, Doku HC, Tally FP. A prospective double-blind evaluation of penicillin versus clindamycin in the treatment of odontogenic infections. J Oral Maxillofac Surg. 1988;46:1065–1070.
  30. Sandor G, Low DE, Judd PL, Davidson RJ. Antimicrobial treatment options in the management of odontogenic infections. J Can Dent Assoc. 1998;64:508–514.
  31. Drusano GL. Antimicrobial pharmacodynamics: critical interactions of ‘bug and drug.’ Nat Rev Microbiol. 2004;2:289–300.
  32. Martinez MN, Papich MG, Drusano GL. Dosing regimen matters: the importance of early intervention and rapid attainment of the pharmacokinetics/pharmacodynamics target. Antimicrob Agents Chemother. 2012;56:2795–2805.
  33. Bahcall JK. Everything I know about endodontics, I learned after dental school, Part 2. Dent Today. 2003;22:62–68.
  34. Newman M, Kornman K. Antibiotics/Antimicrobial Use in Dental Practice. Chicago: Quintessence;1984:152.

Featured photo by BAGI1998/IE+/GETTY IMAGES PLUS

From MENTOR. October 2017;8(10): 24, 26, 28, 30.

Add a Comment

NYU Dentistry Study Finds Evidence That Protein MCP-1 May Determine Bone Loss Responses to Parathyroid Hormone
UConn Professor Honored for Prosthodontic Humanitarian Efforts
Stephen Hudis Sworn in as Vice President of the American College of Prosthodontists
Crosstex Expands Product Portfolio with Acquisition of SAFE-FLO Saliva Ejector Products