References

Martin EA, 7th edn. New York: Oxford University Press Inc; 2007
O'Keefe EM Pain in endodontic therapy: preliminary study. J Endod. 1976; 2:315-319
Georgopoulou M, Anastassiadis P, Sykaras S Pain after chemomechanical preparation. Int Endod J. 1986; 19:309-314
Pak JG, White SN Pain prevalence and severity before, during, and after root canal treatment: a systematic review. J Endod. 2011; 37:429-438
Yu C, Abbott PV An overview of the dental pulp: its functions and responses to injury. Aust Dent J. 2007; 52:4-16
Tønder KJ, Kvinnsland I Micropuncture measurements of interstitial fluid pressure in normal and inflamed dental pulp in cats. J Endod. 1983; 9:105-109
Oguntebi BR, DeSchepper EJ, Taylor TS, White CL, Pink FE Postoperative pain incidence related to the type of emergency treatment of symptomatic pulpitis. Oral Surg Oral Med Oral Pathol. 1992; 73:479-483
Abbott PV, Yu C A clinical classification of the status of the pulp and the root canal system. Aust Dent J. 2007; 52:S17-S31
Hargreaves KM, Cohen S, Berman LH, 10th edn. Oxford: Mosby Elsevier; 2010
Polycarpou N, Ng YL, Canavan D, Moles DR, Gulabivala K Prevalence of persistent pain after endodontic treatment and factors affecting its occurrence in cases with complete radiographic healing. Int Endod J. 2005; 38:169-178
Gotler M, Bar-Gil B, Ashkenazi M Postoperative pain after root canal treatment: a prospective cohort study. Int J Dent. 2012;
Hasselgren G, Reit C Emergency pulpotomy: pain relieving effect with and without the use of sedative dressings. J Endod. 1989; 15:254-256
Rosenberg PA, Babick PJ, Schertzer L, Leung A The effect of occlusal reduction on pain after endodontic instrumentation. J Endod. 1998; 24:492-496
Parirokh M, Rekabi AR, Ashouri R, Nakhaee N, Abbott PV, Gorjestani H Effect of occlusal reduction on postoperative pain in teeth with irreversible pulpitis and mild tenderness to percussion. J Endod. 2013; 39:1-5
Kim S Neurovascular interactions in the dental pulp in health and inflammation. J Endod. 1990; 16:48-53
Gatchel RJ Managing anxiety and pain during dental treatment. J Am Dent Assoc. 1992; 123:37-41
Birchfield J, Rosenberg P Role of the anesthetic solution in intrapulpal anesthesia. J Endod. 1975; 1:26-27
Hargreaves KM, Keiser K Local anesthetic failures in endodontics. Endod Topics. 2002; 1:26-39
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
Mikesell P, Nusstein J, Reader A, Beck M, Weaver J A comparison of articaine and lidocaine for inferior alveolar nerve blocks. J Endod. 2005; 31:265-270
Cohen H, Cha B, Spangberg L Endodontic anesthesia in mandibular molars: a clinical study. J Endod. 1993; 19:370-373
Claffey E, Reader A, Nusstein J, Beck M, Weaver J Anesthetic efficacy of articaine for inferior alveolar nerve blocks in patients with irreversible pulpitis. J Endod. 2004; 30:568-571
McLean C, Reader A, Beck M, Meryers WJ An evaluation of 4% prilocaine and 3% mepivacaine compared with 2% lidocaine (1:100,000 epinephrine) for inferior alveolar nerve block. J Endod. 1993; 19:146-150
Chaney MA, Kerby R, Reader A, Beck FM, Meyers WJ, Weaver J An evaluation of lidocaine hydrocarbonate compared with lidocaine hydrochloride for inferior alveolar nerve block. Anesth Prog. 1991; 38:212-216
Hinkley SA, Reader A, Beck M, Meyers WJ An evaluation of 4% prilocaine with 1:200,000 epinephrine and 2% mepivacaine with 1:20,000 levonordefrin compared with 2% lidocaine with: 100,000 epinephrine for inferior alveolar nerve block. Anesth Prog. 1991; 38:84-89
Nusstein J, Reader A, Beck M Anesthetic efficacy of different volumes of lidocaine with epinephrine for inferior alveolar nerve blocks. Gen Dent. 2002; 50:372-375
Hannan L, Reader A, Nist R, Beck M, Meyers WJ The use of ultrasound for guiding needle placement for inferior alveolar nerve blocks. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1999; 87:658-665
Goldberg S, Reader A, Drum M, Nusstein J, Beck M Comparison of the anesthetic efficacy of the conventional inferior alveolar, Gow-Gates, and Vazirani-Akinosi techniques. J Endod. 2008; 34:1306-1311
Montagnese T, Reader A, Melfi R A comparative study of the Gow-Gates technique and a standard technique for mandibular anesthesia. J Endod. 1984; 10:158-163
Martínez González JM, Benito Peña B, Fernández Cáliz F, San Hipólito Marín L, Peñarrocha Diago M A comparative study of direct mandibular nerve block and the Akinosi technique. Medicina Oral. 2003; 8:143-149
Clark S, Reader A, Beck M, Meyers WJ Anesthetic efficacy of the mylohyoid nerve block and combination inferior alveolar nerve block/mylohyoid nerve block. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1999; 87:557-563
Kaufman E, Weinstein P, Milgrom P Difficulties in achieving local anesthesia. J Am Dent Assoc. 1984; 108:205-208
Kanaa MD, Meechan JG, Corbett IP, Whitworth JM Speed of injection influences efficacy of inferior alveolar nerve blocks: a double-blind randomized controlled trial in volunteers. J Endod. 2006; 32:919-923
Bangerter C, Mines P, Sweet M The use of intraosseous anesthesia among endodontists: results of a questionnaire. J Endod. 2009; 35:15-18
Walton R, Abbott B Periodontal ligament injection: a clinical evaluation. J Am Dent Assoc. 1981; 103:571-575
Aggarwal V, Jain A, Kabi D Anesthetic efficacy of supplemental buccal and lingual infiltrations of articaine and lidocaine after an inferior alveolar nerve block in patients with irreversible pulpitis. J Endod. 2009; 35:925-929
Ashraf H, Kazem M, Dianat O, Noghrehkar F Efficacy of articaine versus lidocaine in block and infiltration anesthesia administered in teeth with irreversible pulpitis: a prospective, randomized, double-blind study. J Endod. 2013; 39:6-10
Reisman D, Reader A, Nist R, Beck M, Weaver J Anesthetic efficacy of the supplemental intraosseous injection of 3% mepivacaine in irreversible pulpitis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1997; 84:676-682
Nusstein J, Kennedy S, Reader A, Beck M, Weaver J Anesthetic efficacy of the supplemental X-tip intraosseous injection in patients with irreversible pulpitis. J Endod. 2003; 29:724-728
Bigby J, Reader A, Nusstein J, Beck M, Weaver J Articaine for supplemental intraosseous anesthesia in patients with irreversible pulpitis. J Endod. 2006; 32:1044-1047
Replogle K, Reader A, Nist R, Beck M, Weaver J, Meyers WJ Cardiovascular effects of intraosseous injections of 2 percent lidocaine with 1:100,000 epinephrine and 3 percent mepivacaine. J Am Dent Assoc. 1999; 130:649-657
Birchfield J, Rosenberg P Role of the anesthetic solution in intrapulpal anesthesia. J Endod. 1975; 1:26-27
VanGheluwe J, Walton R Intrapulpal injection – factors related to effectiveness. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1997; 19:38-40
Nakanishi T, Shimizu H, Hosokawa Y, Matsuo T An immunohistological study on cyclooxygenase-2 in human dental pulp. J Endod. 2001; 27:385-388
Dale MM, Rang HP, Dale MM, 7th edn. Edinburgh: Churchill Livingstone; 2007
Clark DW, Layton D, Shakir SA Do some inhibitors of COX-2 increase the risk of thromboembolic events? Linking pharmacology with pharmacoepidemiology. Drug Saf. 2004; 27:427-456
Hargreaves KM, Keiser K, Byrne E Endodontic pharmacology. In: Cohen S, Hargreaves KM St Louis: Mosby; 2005
(Accessed January 2014)
Barden J, Edwards JE, McQuay HJ, Wiffen PJ, Moore RA Relative efficacy of oral analgesics after third molar extraction. Br Dent J. 2004; 197:407-411
Ahmad N, Grad HA, Haas DA, Aronson KJ, Jokovic A, Locker D The efficacy of nonopioid analgesics for postoperative dental pain: a meta-analysis. Anesth Prog. 1997; 44:119-126
Menhinick KA, Gutmann JL, Regan JD, Taylor SE, Buschang PH 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; 37:531-541
Weil K, Hooper L, Afzal Z, Esposito M, Worthington HV, van Wijk AJ Paracetamol for pain relief after surgical removal of lower wisdom teeth. Cochrane Database Syst Rev. 2007;
Melbourne: Therapeutic Guidelines Ltd; 2002
Keiser K, Hargreaves KM Building effective strategies for the management of endodontic pain. Endod Top. 2002; 3:93-105
Walton RE, Chiappinelli J Prophylactic penicillin: effect on post treatment symptoms following root canal treatment of asymptomatic periapical pathosis. J Endod. 1993; 19:466-470
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
Jebeles JA, Reilly JS, Gutierrez JF, Bradley EL, Kissin I Tonsillectomy and adenoidectomy pain reduction by local bupivacaine infiltration in children. Int J Pediatr Otorhinolaryngol. 1993; 25:149-154
Gordon SM, Dionne RA, Brahim J, Jabir F, Dubner R Blockade of peripheral neuronal barrage reduces postoperative pain. Pain. 1997; 70:209-215
Woolfe C Evidence for a central component of post-injury pain hypersensitivity. Nature. 1983; 306
McQuay H Do pre-emptive treatments provide better pain control. In: Gebhardt GF, Hammond DL, Jemsen TS Seattle: IASP Press; 1994
Dionne R To tame the pain?. Compend Contin Educ Dent. 1998; 19:421-426
Adelson D, Goldfried M Modeling and the fearful child patient. J Dent Child. 1970; 37:476-488
Chaves JF, Barber TX Cognitive strategies, experimenter modelling and expectation in the attention of pain. J Abnormal Psych. 1974; 83:316-363
Gatchel RJ Managing anxiety and pain during dental treatment. J Am Dent Assoc. 1992; 123:37-41

Effective pain management strategies in endodontic therapy

From Volume 43, Issue 6, July 2016 | Pages 575-587

Authors

Satnam Singh Virdee

BDS, MFDS RCSEd

Dental Core Trainee, Restorative Dentistry, Leeds Dental Institute, Clarendon Way, Leeds, West Yorkshire LS2 9LU, UK

Articles by Satnam Singh Virdee

Abstract

Pain management is the key to providing successful root canal therapy. All patients hope for a painless procedure and look forward to being free of their symptoms when treatment is complete. However, managing pain throughout endodontic therapy can be challenging and improving awareness of various analgesic techniques can make a significant difference to both patient and practitioner. This article should provide some insight into these methods and use current literature to discuss how they can be delivered in a clinical setting. By doing so, practitioners can utilize these techniques to make endodontic treatment a more comfortable procedure.

CPD/Clinical Relevance: This article aims to improve the reader's awareness of the various clinical, pharmacological and behavioural analgesic techniques that can be used to help control presenting symptoms, reduce iatrogenic-induced pain and manage post-operative discomfort in the endodontically compromised patient.

Article

Pain is a common symptom that brings many patients to the dentist but in some cases keeps them away due to fear and anxiety. The Oxford Medical Dictionary defines pain as ‘an unpleasant sensation ranging from mild discomfort to agonized distress associated with real or potential tissue damage'.1 Dental care has become linked to this unpleasant definition and has regrettably developed into a common public perception. However, it can be argued that endodontic therapy is a prime contributor to this physiological and psychological discomfort and, although these procedures intend to eliminate symptoms, pain relief may rarely be instantly achieved.2 Strong evidence supports this link and, if we are to deliver higher standards of care, we must be aware of strategies to prevent, minimize and control pain before, during and after endodontic therapy.3,4 This article explores various tools within the dentist's armamentarium that offer help in managing pain and how to utilize them to allow for a comfortable endodontic procedure.

Pathophysiology of endodontic pain

Pulpitis commences when a carious lesion passes the amelo-dentinal junction and enters into dentine.5 Initially, acidic bacterial by-products, that enter the pulp before the micro-organisms, cause inflammatory cell localization, slightly raising pulpal haemo-dynamic pressures.5 This stimulates Ad nociceptors, resulting in a pain typical of reversible pulpitis.5

Bacterial invasion into the pulp induces profound pulpal inflammation which stimulates the deeper C nociceptors.5 This causes neuropeptide (Substance P) and inflammatory cytokine (PGE-2) release, drastically impacting pulpal vasculature.5 The increase in hyperaemia, vascular permeability and localization of inflammatory cells amplifies pulpal haemo-dynamic pressures.5 The rigid walls of the root canal system do not accommodate this change and the vasculature collapses, resulting in hypoxia and bringing about irreversible pulpitis and pulpal necrosis.5

This pulpal strangulation theory proposes inflammation is generalized throughout the pulp, however, Tønder suggests that it is a more localized event (Figure 1).6

Figure 1. The inflamed dental pulp. This study demonstrated that there is only a localized increase in pulpal hydrostatic pressures in response to inflammation in the pulp. However, the pulp of cats' teeth was used to collect this data and so one may question how much this applies to the human pulp.6

Further research would improve our clinical understanding of this which, in turn, enhances our clinical management.

Examination

Diagnosis

Arriving at an accurate diagnosis is the first step in managing oro-facial pain. It serves a vital purpose in helping us to identify the aetiology of presenting symptoms, communicate between colleagues and determine the appropriate treatment options. This can be challenging and is the pivotal moment in determining if pain will be effectively controlled. Therefore, the importance of accuracy can be appreciated as an incorrect diagnosis can lead to incorrect treatment. For example, if a lateral periodontal abscess is misdiagnosed as an apical abscess, endodontic treatment would be indicated when in fact a far more conservative approach is required. Furthermore, the presenting symptoms would still persist until the correct treatment was provided.

For endodontic purposes, we are specifically concerned with arriving at a pulpal and apical diagnosis.7 Therefore, it would be useful to adopt a simple and practical classification system where diagnostic terms represent clinical findings. A good example of this is the classification set out by Abbott and Yu which depicts the progressive nature of pulpal and apical pathology.8 Furthermore, each histo-pathological diagnostic term is defined by clinical findings and the appropriate management strategy is clearly outlined.

When patients arrive in pain, the following information should be methodically acquired through systematic history-taking, thorough clinical examination and appropriate special investigations:

  • Is the pain odontogenic or nonodontogenic?
  • Is the tooth vital or non-vital?
  • Is the pain of pulpal or periradicular origin, or both?
  • Is the pain primarily inflammatory or infectious?
  • Is there a periodontal component?
  • Is the pain reproducible?
  • When the necessary information is collected, we can begin to form our definitive diagnosis followed by a treatment plan. It is important to appreciate the dynamic nature of the pathology in these tissues and occasions will occur where clinical findings contradict each other. If we are unable to arrive confidently at a diagnosis we should seek a second opinion or refer to an experienced practitioner.

    Predictive models of pain

    Is it possible to identify individuals that are more likely to experience pain throughout treatment? The evidence may suggest, as several pre-operative risk factors have demonstrated, a consistent link with post-operative discomfort. After Hargreaves carried out a literature review containing approximately 12,000 patients, it was determined that hyperalgesia and tenderness to mechanical stimulation were shown to be the most significant predictors of postoperative pain.9 Interestingly, other findings that showed a weaker correlation were the presence of apical pathology, a necrotic pulp and carrying out endodontic therapy in two stages.9 Several studies have also pointed to a more detailed relationship, concluding that particular presenting symptoms had an effect on the intensity and duration of the pain felt after treatment (Table 1).


    Characteristic Risk Factors Evidence
    Presence
  • Pre-operative pain: 100%
  • Tender to percussion: 100%
  • Sex: female: 38%
  • One stage endodontics: 33%
  • Apical periodontitis: 31%
  • Necrotic pulp: 25%
  • Hargreaves et al, 20109
    Intensity
  • Intensity of pre-operative pain
  • Vital pulp
  • O'Keefe, 19762Gotler, Bar-Gil and Ashkenazi, 201211
    Duration
  • Pre-operative pain > 3 months
  • Tender to percussion
  • Chronic pain patients
  • Previous painful orofacial treatment
  • Sex: female
  • Polycarpou et al, 200510

    Clinical strategies

    Pulpotomy or pulpectomy

    These procedures are effective clinical methods for directly treating the pathological causes of the patient's symptoms. A pulpotomy is the removal of diseased coronal pulp tissue whilst maintaining vitality of healthy radicular tissue. A pulpectomy is the complete removal of both coronal and radicular pulpal tissue.

    Pulpotomy

    A pulpotomy is indicated to manage an irreversibly inflamed pulp when there is limited time to carry out a pulpectomy in teeth with no swelling. Accessing the pulp counteracts rises in local tissue pressures, whilst removing the necrotic coronal pulp severs nociceptive nerves that respond to inflammatory mediators. Introducing therapeutic dressings over the remaining radicular pulp reduces the inflammatory mediator concentration and sealing the tooth prevents bacterial recontamination. Clinical trials suggest it's a combination of caries removal, pulpotomy and effective coronal seal that provides significant analgesia as opposed to the type of pulpal dressing applied.12

    A partial pulpectomy, the incomplete debridement of radicular tissue, results in radicular tissue damage, haemorrhaging and residual necrotic debris which results in greater post-operative pain. Clinical trials demonstrate higher incidences of post-operative pain in teeth diagnosed with irreversible pulpitis after a partial pulpectomy as opposed to a pulpotomy.3,7 Therefore, when time does not permit, a pulpotomy will provide sufficient analgesia and partial pulpectomy should be avoided.

    Pulpectomy

    A pulpectomy is prescribed for those presenting with symptoms of irreversible pulpitis with or without apical involvement. It involves chemo-mechanical debridement of the coronal and radicular pulp removing noxious stimuli that would otherwise induce inflammation. It is then followed by a temporary dressing (ie non-setting calcium hydroxide) that acts on any residual bacteria. Due to the impossible nature of clinically determining the extent of pulpal pathosis, this procedure provides the advantage in that the entire pulp is simply removed. However, accuracy is important and, without correct canal measurements, a partial pulpectomy may be inadvertently performed leading to its associated risks of post-operative pain.3,7

    Although the mechanism of providing pain relief differs, either a pulpotomy or pulpectomy are effective clinical strategies in controlling acute endodontic pain. Selection depends on the time available but a partial pulpectomy should be avoided. These procedures should be considered as a first point of analgesia in emergency patients as they treat both the symptoms and the pathology as opposed to relying on pharmacological methods that only treat the former.

    Occlusal reduction

    Having once been considered common practice amongst endodontically compromised teeth, the true benefit of occlusal reduction has been open for debate. Rosenberg et al discovered that teeth exhibiting pulp vitality, sensitivity to percussion, pre-operative pain and/or no periapical radiolucency on presentation, were statistically proven to gain the greatest chance of pain relief with occlusal reduction (Figure 2).13 It was concluded that any one of these signs/symptoms was enough to warrant occlusal reduction. Although there was an extensive exclusion criterion, a large sample size and the statistical significance, the findings cannot be ignored.

    Figure 2. Occlusal reduction in reducing pain. Reproduced with permission from: Rosenberg et al. The effect of occlusal reduction on pain after endodontic instrumentation. J Endod 1998; 24: 492–496.13

    Recently, Rosenberg's findings have been challenged. Parirokh et al concluded that ‘Occlusal surface reduction did not provide any further reduction in post-operative pain for teeth with irreversible pulpitis and mild tenderness to percussion compared with no occlusal reduction'.14 Although results were statistically significant, no power calculation was used to determine the sample size, which was small, and there was also an uneven dropout rate between groups.

    Our biological understanding of the surrounding periodontium may provide help. Irritation to the periodontal tissues (ie over instrumentation, infection) releases inflammatory cytokines that sensitize peripheral nociceptive nerve fibres at the periphery of the periodontal ligament and pulp. Therefore, any subsequent mechanical stimulation (ie occlusal loading) will stimulate both proprioceptive and sensitized nociceptive fibres, resulting in pain.15 Therefore, theoretically the anatomy does suggest a link.

    Although there is contrasting research, compromised teeth presenting with the profile outlined by Rosenberg may benefit from occlusal reduction.

    Pharmacological strategies

    Local anaesthetics

    An essential form of pain management is the ability to achieve profound pulpal anaesthesia for appropriate durations of time. The membrane stabilizing theory of local anaesthetics is well understood, however, we know that achieving anaesthesia is not just dependent on the anaesthetic but also the patient.16 There are those who have slower onsets and others that do not respond even after 60 minutes, despite the growing number of techniques and solutions available.17 The following section highlights practices that could help achieve appropriate anaesthesia in even the most difficult scenarios.

    Teeth diagnosed with irreversible pulpitis should be approached with caution, especially the mandibular molar. These teeth have undeniably posed anaesthetic challenges to the dentist and are referred to by some as the ‘HOT TOOTH’ (Figure 3).18 Reports found objective sensibility tests were less reliable and operative pain was still experienced after consecutive negative readings.19 A single Inferior Dental Block (IDB) in a hot mandibular molar may not always achieve adequate pulpal anaesthesia and supplemental techniques may be needed for a greater chance of success.18

    Figure 3. Irreversible pulpitis and pulpal anaesthesia.18

    Upon failing to achieve pulpal anaesthesia in an irreversibly inflamed mandibular molar, dentists may find themselves questioning their technique, wondering if different anaesthetic preparations will help or if simply greater volumes are needed. However, repeated clinical trials fail to highlight superiority of various anaesthetic preparations (including articaine-4%) over lidocaine-2% epinephrine-1:100000 when applied to nerve blocks.20,21,22,23,24,25 Similarly, increasing volumes of anaesthetic or epinephrine concentration has no impact and giving a repeat injection following a failed IDB will only cause further discomfort.26 Although technical inaccuracy can account for a percentage of failures, when Hannan et al used ultrasound to guide the needle to a precise location during an IDB, there was no statistical improvement in rate of pulpal anaesthesia achieved.27 In addition, numerous clinical trials have failed to provide evidence to support the superiority of Gow-Gates or Vazirani-Akinosi techniques over conventional IDB techniques.28,29,30 Therefore, accuracy cannot be the primary reason for failure and accessory nerve supply from the mylohyoid nerve does not seem to be a significant barrier either.31

    Prior to treatment, an accurate history should be taken as those previously experiencing difficulty in getting numb have reduced chances of success.32 During administration, slower injections (60 seconds) are less painful and have proven to be more successful than rapid IDBs in healthy mandibular molars.33 Following this, efforts to test pulpal anaesthesia objectively (ie thermal/electrical stimuli) should be made. It is common practice to probe the gingiva with sharp instruments, ask if the lip feels numb or even to start treatment and wait for a response to assess the degree of anaesthesia. However, these subjective methods are inaccurate representations of assessing pulpal anaesthesia.23,24,25 It is suggested that true pulpal anaesthesia occurs in teeth exhibiting two consecutive negative readings at strengths of 80, on an analytic pulp tester, within 15 minutes and sustaining these readings for 60 minutes. Although this may seem impractical, it is the standard used in numerous studies.23,24,25

    Failure to position the needle accurately will result in failure of subjective signs (ie lip numbness) prompting a second attempt. However, when subjective signs are present and the pulp remains unaffected, supplemental techniques have been shown to be helpful. The most common of these is the Intra-Ligamentary (IL) injection.34 Figures show that the technique aids achieving pulpal anaesthesia by ~75% initially and ~95% upon reinjection, with a modest rate of ~55% in patients presenting with irreversible pulpitis.21,35 Achieving back pressure is essential to success and, without it, anaesthesia would be unlikely to occur.35 Reports of buccal infiltrations with articaine-4% epinephrine-1:100000 alongside IDBs have been demonstrated to be more clinically significant.36,37 However, it too suffers the same fate when it comes to the hot tooth, with reports of only 58% achieving pulpal anaesthesia.35

    The uncommon but gold standard Intra-Osseous (IO) technique provides immediate pain relief which can last for up to 60 minutes. Numerous clinical trials have demonstrated promising results even with patients presenting with hot teeth.38,39,40 Reisman confirmed profound pulpal anaesthesia in 80% of initial IO injections and 96% after reinjection in irreversibly inflamed teeth following a failed IDB.38 One must be mindful of the transient increase in heart rate, especially with medically compromised patients, however, mepivacaine-3% IO injections have proven to overcome such matters.41

    Finally, 5–10% of mandibular posterior teeth diagnosed with irreversible pulpitis will be unresponsive to even repeat supplemental injections.42,43 This indicates administration of intra-pulpal anaesthesia via a conventional needle. Although initially uncomfortable, the instant pain relief for a short duration allows the operator a small window to debride the pulp chamber, offering some pain relief.

    Analgesics

    A temporary method of pain management is the use of analgesics. With an extensive range available, it can be confusing to prescribe the correct regimen that is both effective and bares little consequences to an ageing population. The following discusses some common analgesics and flexible regimens that can be used for endodontic related pain.

    Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

    Higher expressions of cyclooxygenase-2 (COX) enzymes in the pulp of teeth diagnosed with irreversible pulpitis make NSAIDs effective tools for managing dental pain.44 Their ability to inhibit COX-1&2 enzymes stops inflammatory cytokine production and reduces inflammation to provide analgesia.45 However, their unselective nature means that adverse effects (ie gastrointestinal disturbances), mainly due to COX-1 inhibition, are witnessed and are contra-indicated in medically compromised patients (asthma, renal failure), with recent reports linking selective COX-2 inhibitors to thrombo-embolic events.45,46 The relatively safe nature and extensive research of Ibuprofen has made it the NSAID of choice.47 Multiple, double-blinded, placebo-controlled clinical trials demonstrate its efficacy in managing post-operative pain (Table 2). It has a dose-dependant nature and greatest analgesia is experienced at 800 mg, 1–2 hours after administration.48


    Paracetamol/Acetaminophen

    Although the centralized action of paracetamol is poorly understood, its use provides analgesia and anti-pyrexia. Its lack of peripheral action at therapeutic doses means that there's no anti-inflammatory effect and there are fewer side-effects, making it ideal when NSAIDs are contra-indicated. However, one must be mindful of possible hepatotoxicity and liver-related illnesses.45 A Cochrane review found the maximum benefits were experienced at 1000 mg dosages every 6 hours post-treatment, with an onset of 30–60 mins after administration.52

    Opioids/opioid combinations

    Opioids block only the perception of pain by inhibiting opiate receptors in the CNS and they have no anti-inflammatory effects.45 At 60 mg, codeine's significant analgesic effect can be experienced, all be it less than that of paracetamol (600 mg) and aspirin (650 mg).48 Due to this weak effect, it is often used in combination with non-narcotic analgesics. Codeine (8–30 mg) alongside paracetamol (500 mg) has been reported to provide greater analgesia than paracetamol alone, but less than that of Ibuprofen.48 There is little evidence that discusses codeine's effective analgesic dose alongside paracetamol, but suggestions of at least 25–30 mg have been put forward, implying that 8–10/500 preparations are not ideal.53 The CNS depressant side-effects of codeine should be taken into account when prescribing.

    Drugs should only be prescribed as temporary forms of pain relief for approximately 24–48 hours, whilst the aetiology is managed. Ibuprofen is the drug of choice and, where contra-indicated, paracetamol-codeine preparations can be used as part of a flexible regimen (Table 3).4 Furthermore, they can be taken together to provide continuous pain relief (Figure 4).51,54 Antibiotics have no measurable impact in managing or preventing post-operative pain and so should only be prescribed in accordance with guidelines.54,55,56


    Figure 4. Continuous pain relief regimen.

    Pre-emptive pharmacological strategies

    Pre-emptive anaesthesia

    Long-acting local anaesthetics (Bupivicaine) have been shown to be useful in providing post-operative analgesia.57,58 When administered as a block, there is less nociceptive afferent barrage which has been shown to induce central hyperalgesia.59 Subsequently, patients experience a delayed onset, less use of analgesic medications and less pain 2–7 days after the procedure.57,58 If anticipating a short procedure it can be administered pre-operatively, however, for longer treatments, it is best administered post-operatively.

    Pre-emptive analgesia

    Pre-operative NSAID use has also been shown to reduce the onset and intensity of post-operative pain.60 This can account for their ability to inhibit production of inflammatory mediators in the pulp, as discussed earlier. However, this strategy can only be used in patients that can tolerate NSAIDs as paracetamol does not provide the same anti-inflammatory effect.

    Pre-emptive analgesics and anaesthetics have clear benefits in controlling the onset and intensity of postoperative pain. When combined it has been shown to have marked additive effects and so this strategy can be an effective form of pain management.61

    Behavioural strategies

    Although physiological elements of pain are well understood, psychological components vary from individual to individual, resulting in its subjective nature. Numerous studies have established the close relationship between dental anxiety and pain.16 However, with the correct care, an opportunity to break this association can be created without the need for pharmacological agents.

    Patients should be greeted with a welcoming tone and body language as the initial contact will have a direct effect on their anxiety. Pre-operatively, all relevant information should be provided, including risk of post-operative pain and flare ups. Videos or observing individuals undergoing treatment are also useful in providing information. Distraction techniques are commonly used for pre-occupation during treatment, reducing the patient's focus on the anxiety. These techniques all provide the patient with a greater sense of control and have been shown to reduce anxiety in several studies.62,63,64

    The dentist should exercise these behavioural strategies where possible, not only for pain management but also to allow for a smooth, uninterrupted endodontic procedure.

    Conclusion

    Pain management is the key to providing successful root canal therapy and all patients look forward to being free of their symptoms once the appointment is complete. Although this expectation may place stress on both parties, a combination of clinical, pharmacological and behavioural techniques, such as those described above, have demonstrated their efficacy to achieve this goal. However, the approach must be tailored to the needs of each individual, which relies on the dentist's professional judgement. Current interventions alongside new advancements are making endodontic therapy an ever more comfortable experience.