OralSurgery

Nadine Khawaja

Tara Renton Part 3: Acute

Abstract: Acute trigeminal pain is a common presentation in the dental surgery, with a reported 22% of the US adult population experiencing orofacial pain more than once during a 6-month period.1 This article discusses the mechanisms underlying the pain experience, diagnosis and subsequent management of acute trigeminal pain, encompassing pre-, peri- and post-operative analgesia. The dental team spend most of their working lives managing patients and acute pain. The patient may present to the clinician in existing pain, which may often provide a diagnostic challenge. Prevention and managing intra-operative and post-surgical pain are implicit in providing your patient with optimum care. CPD/Clinical Relevance: This paper aims to provide an overview of conditions that may present with acute orofacial pain and their management using the most recent evidence base. Intra-operative and post-surgical are also scrutinized and evidence- based treatment is recommended. Dent Update 2015; 42: 442–462

‘A , or a violent passion, is not empathy and patience. Oral trigeminal . Pain has a dramatic necessarily diminished by our knowledge are commonly prescribed for a few days physiologic impact that can adversely of its causes, its character, its importance or following oral surgery or other procedures, affect the health and well-being of dental insignificance’ wrote T S Eliot. after which patients are typically pain-free patients.5 Furthermore, if acute pain is not Acute pain management is or can switch to over-the-counter (OTC) treated adequately, there is a risk that it integral to the provision of optimal dental medications (ie either lower doses of the may become chronic in nature. Therefore, care and supporting the well-being of same analgesics or different OTC drugs). adequate pain control is a medical and patients. Any patient attending a dentist Acute trigeminal pain is a dental necessity and not merely an issue of will be experiencing some degree of anxiety distressing, common encompassing pain patient comfort. and stress. These emotions will lower from the orofacial region and head.2 It is now understood that the patient’s and further A cross-sectional population study in early control of acute pain can shape its compound pain management. Anyone in Cheshire, England, reported that orofacial subsequent progression, by preventing this field recognizes that pain is complex, pain (OFP) affected a quarter of the nociceptive input and, hence, preventing particularly in the dental environment population, of whom only a half sought persistent pain.6 Good pain management where , phobia and poor expectations help.3 The prevalence was higher in women can help prevent the negative physiological compound the patient’s pain experience. and younger adults (18–25 years) with 17% (tachycardia, hypertension, myocardial Dentists require an armamentarium of of the population having time off work ischaemia, decrease in alveolar ventilation, psychological, communication, medical and or unable to carry out normal activities and poor wound healing) and psychological technical skills. Managing operative pain due to the pain.3 The impact of pain on (anxiety, sleeplessness, phobia) outcomes.5 under local anaesthesia requires expertise, the economy is demonstrated by a cross- Management of acute dental sectional survey in eight countries in Europe pain includes management of patients which estimated the total annual cost of undergoing surgery (peri- and post- among adults, aged 18 to 65 operative) and those presenting with pain Nadine Khawaja, BDS, MJDF years, as €173 billion.4 as a result of underlying pathology (eg MSurgDent, Specialist Academic Trainee, The dental profession, since its , ulcer). Patients with trigeminal pain Department of Oral Surgery and Tara infancy, has been a pioneer in the fields may often present to dental practitioners. Renton, BDS, MDSc, PhD, FARCDS(OMS) of anaesthesia and pain control. This Successful management of acute trigeminal FDS, RCS FHEA, Professor of Oral stems from the need for these modalities pain is dependent on obtaining a correct Surgery, King’s College London Dental to render painless dental care in an diagnosis of the source of pain.7 This is Institute, King’s College Hospital London, anatomic region that is highly innervated achieved through comprehensive history- Bessemer Road, London SE5 9RS, UK. by the second and third divisions of the taking, examination and appropriate 442 DentalUpdate June 2015 OralSurgery

special tests (Table 1). Initial history- taking into account associated signs Management of acute taking should include determining the and symptoms, radiation, functionality, trigeminal pain site, onset, character (type of pain), disability, psychological effects and time The management of acute 7 severity (verbal/numerical, Table 2) and course. Management of acute pain as a trigeminal pain can be divided into three any exacerbating/relieving factors. A presentation symptom is discussed in later areas: intra-operative, post-operative and thorough assessment can be completed articles. acute symptomatic pain (usually acute

Diagnostic Requirements

Identify signs of Redness, swelling, heat pain, loss of function Response to anti-inflammatory drugs (eg NSAIDs) Response to antibiotics if initiated by infection

Loss of function , inability to bite on , difficulty swallowing

Special tests (Endofrost/ Electric NB Surrogate measure of vitality as it measures nerve response rather than condition of test/heat) blood supply Non response does not always signify pulpal Positive response may be complicated in multi-rooted teeth with varying pulpal conditions in different canals Short sharp pain, which doesn’t linger (ie Ad fibre mediated) suggests inflammation is superficial in the pulp and, therefore, can be reversible Lingering, dull, aching poorly localized pain (ie C-fibre mediated pain) is suggestive that the inflammatory process has spread to the central part of the pulp and, therefore, the pulp is irreversibly inflamed Pain on release of biting may indicate ‘’ using a ‘tooth sleuth’ or simply a cotton roll between the tooth cusps

Neuropathic signs Mechanical (pain to stimulus which is not normally painful eg light touch) (increased pain to painful or )

Radiographs Long Cone periapical using paralleling technique for individual to three teeth in single quadrant Bitewing radiographs If multiple quadrants or impacted teeth use dental panoramic tomography (DPT) Cone beam computerized tomography (CT) for localization of high risk teeth or impacted teeth

Haematological investigations CRP levels in acute spreading infections ESR for , pain of unknown aetiology

FBC with Haematinics (Fe, B12, Folate) Zinc (required for Fe absorption) Thyroid function tests HBA1c (exclude ) Auto-antibody screen (ENAs and ANAs)

Biopsy Punch, classical, laser biopsy for lesions of unknown aetiology for histopathological diagnosis

Signs of sinister disease Over 50 years Sudden recent onset, intense pain Painless trismus, worsening trismus despite therapy Neuropathy Asymmetry

Table 1. History, examination and special tests.

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Pain assessment tool Assessment

Category rating scale Choice of five categories: None, Mild, Moderate, Severe, Unbearable

Visual analogue scale (VAS) Draw a line from no pain to worst pain

No pain Worst pain

Numerical rating scale Choose a number from 1–10

1 2 3 4 5 6 7 8 9 10 No pain Worst pain

Table 2. Summary of pain assessment tools. infection). They are quick and easy to use (Table of nerve depolarization and firing. The 1. Management of intra-operative pain: 2),8 whereas pain questionnaires can membrane expansion theory suggests management of anxiolysis, non-medical often assess the quality and character of non-specific swelling of the cell membrane (behavioural) and medical (sedation) is not the pain (eg McGill Pain Questionnaire by absorption of the LA, whilst the newer covered in depth in this article; (MPQ)), as well as its intensity.9 The MPQ specific binding theory describes binding of 2. Management of post-surgical pain; consists primarily of three major classes LA to a specific binding site of the sodium 3. Management of acute orofacial pain: of word descriptors; sensory, affective and channel. Discovery of specific drug binding patient presenting with dental pain as a evaluative to specify the pain experience.8 sites allows for the possibility of developing symptom. anaesthetics with greater sensitivity for The mechanism, peripheral specific sodium channels with reduced side- mediators, central modulation and the Management of intra-operative pain effects.12 trigeminal anatomy of pain have been Local anaesthesia (LA) is is the most commonly covered in Part 1 of this series. fundamental for pain control in outpatient administered local anaesthetic by dental oral surgery and dental procedures. Local practitioners, although other available anaesthetic is defined as a drug which solutions (prilocaine, mepivacaine and Pain assessment reversibly prevents transmission of the articaine) offer advantages in certain The clinician is beholden to nerve impulse in the region to which it is situations (Table 3). In the severely medically- 10 take a full and comprehensive history applied, without affecting consciousness. It compromised patient, such as those with to build trust and understanding of the is frequently used to control intra-operative unstable , an -free solution patient and his/her complaint. Acute pain and immediate post-operative pain. During such as 3% prilocaine with felypressin should will have onset in the last days/weeks and acute tissue trauma mediated pain (eg tooth be used.13 In a meta-analysis, articaine 4% generally has been present for less than 3 extraction), local anaesthetic blocks the pain was found to be superior to lidocaine 2% in months. The pain may be associated with signal transmission to the cerebral cortex, anaesthetizing lower first molars.14 key inflammatory signs (tumor, dolor, calor, preventing pain and processing. Although there are limited rubor and loss of function) but if caused by Hence, local anaesthetic should always be scientific studies in which local anaesthetics a ‘cold bacteria’ may not have the traditional used, even if the patient is under general with higher concentrations (4%) result in inflammatory signs (eg dry socket). Acute anaesthesia, as it prevents nervous system higher incidence of paraesthesia,15 there pain is inflammatory pain responding to sensitization and, hence, reduces post- remains a trend to avoid articaine 4% use 11 anti-inflammatories (eg and operative pain. in (IAN) blocks. Local NSAIDs) and antibiotics, if related to an Local anaesthetic agents bind to anaesthetic related lingual nerve injury is infective cause. sodium channels on , thus inhibiting most likely to occur when multiple inferior There is no absolute measure of the rapid passage of sodium ions and alveolar nerve blocks are given, regardless pain as it is a purely subjective experience. propagation of an action potential. There of the local anaesthetic agent used.16 However, pain assessment is essential in are two theories of the mechanisms of Importantly, buccal infiltration articaine will diagnosing and monitoring a patient’s action of local anaesthetic both of which most likely avoid inferior dental blocks with response to treatment. Pain rating scales involve perturbation of the nerve cell’s lidocaine for most of , also reducing are often used in assessing pain intensity. sodium channels and, hence, prevention the likelihood of IAN LA-related injuries.

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LA solution Vasoconstrictor Duration Use Complications

Lidocaine (2%) 1:80,000 epinephrine Intermediate General dentistry, minor Inferior alveolar nerve oral surgery block (IDB) necessary to Prilocaine (3%) Felypressin Intermediate General dentistry, anaesthetize lower minor oral surgery molar Severely medically compromised patients

Mepivacaine (2%) 1:100,000 epinephrine Intermediate General dentistry, minor oral surgery

Articaine (4%) 1:100,000 epinephrine Intermediate Effective infiltrations to Unfounded claims of anaesthetize ‘Hot’ pulps increased risk to and lower molars (IDN, lingual) during IDB

Bupivacaine (0.5%) 1:200,000 epinephrine Long-acting Oral surgery of long Increased toxicity duration/invasive compared to other procedures, eg osteotomies anaesthetics CNS and cardiovascular adverse effects

Levobupivacaine (0.5%) 1:200,000 epinephrine Long-acting Oral surgery of long Reduced toxicity duration/ invasive compared to procedures, eg bupivacaine osteotomies Table 3. Summary of commonly used local anaesthetics.

Studies have suggested factors are reported to play a significant but rather may limit further production. benefit in using bupivacaine (Marcaine), role in the severity of reported postsurgical Preventive/pre-emptive a long-acting local anaesthetic, to limit pain.22 If patient anxiety prevents the ability analgesia is a treatment that is initiated post-operative pain following third molar to comply with dental procedures under before the surgical procedure to prevent surgery17,18 and endodontic treatment.19 local anaesthesia, then anxiolysis can be and, hence, sensitization of Reports range from a reduction in pain provided using oral, inhalational or IV the peripheral and central pathways.26,27 at 8 hours18 to 7 days17 post-operatively. sedation techniques.23 General anaesthesia Although there are many studies in It is important to note that bupivacaine should be considered if local anaesthesia is general surgery which report the benefits exhibits this property only when used as contra-indicated. of pre-emptive analgesia in reducing the a nerve block and not when used as an post-operative pain experience, there infiltration. Levobupivacaine is a newer Pre-operative analgesia are limited studies in relation to dental anaesthetic solution with an improved Failure of inferior alveolar surgery (see section on NSAIDs), with 28 safety profile than, and equivalent efficacy nerve blocks to anaesthetize teeth with some studies reporting no benefit. Dahl to, bupivacaine (the latter has rare reports symptomatic irreversible pulpitis (‘hot et al highlight the need for improved of causing severe central nervous system pulps’) is partly due to inflammatory design of clinical studies in order to 20 (CNS) and cardiovascular adverse effects). prostaglandin production inducing achieve more conclusive answers A double blind study showed similar peripheral sensitization and regarding the different preventive 26,27 anaesthetic efficacy between bupivacaine central sensitization.24 Studies have interventions. (0.5%) and levobupivacaine (0.5%) in demonstrated that the use of ibuprofen inferior alveolar nerve blocks, suggesting and paracetamol before the inferior alveolar that levobupivacaine is a useful alternative nerve block does not statistically improve Post-surgical pain management 21 to bupivacaine owing to its lower toxicity. success rate.24,25 This is likely to be due Effective post-operative to the fact that sensitization has already pain management is fundamental to Anxiolysis taken place, and NSAIDs cannot reduce the quality dental care, and is likely to speed Cognitive and psychological amount of prostaglandin already present recovery. Conventional analgesics act

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Drug Side-effects (SEs) Mechanism of SE Contra-indications Interactions Alternatives

NSAIDs GI bleeding Erosion of stomach History gastric ulcer/ Anticoagulants Paracetamol (eg ibuprofen & intestine due to gastro-oesophageal (warfarin, clopidogrel), opioids 400 mg, reduced production reflux disease (GORD) SSRIs 50 mg) of protective mucous lining stimulated by PG. Systemic & direct mucosal contact effect

Prolonged bleeding Reduced thromboxane Patients with Anticoagulant Paracetamol A2 reduces platelet bleeding disorders therapy (warfarin, opioids aggregation or on anticoagulant clopidogrel) can therapy, especially increase INR the elderly, have increased risk of severe GI bleed

Nephrotoxicity Reduced renal Patients with Paracetamol function due to compromised renal opioids reduced PG function production which is necessary for renal perfusion

Aspirin/ NSAID Inhibition of COX Individuals sensitive Paracetamol intolerance or shunts arachidonic to subtle elevation opioids allergy pathway toward in leukotrienes – leukotriene synthesis usually asthmatics – signs and Patients allergic symptoms allergic to NSAIDs response eg bronchospasm & anaphylaxis

PGs maintain patency Paracetamol of the ductus arteriosus during foetal development, especially 3rd trimester – avoid in pregnancy

Lithium and Paracetamol methotrexate serum opioids levels elevated during concurrent NSAID use

Paracetamol Liver & kidney Overdose – can result Hepatic impairment Increased INR may Check with damage when taken in hepatotoxicity chronic alcoholism occur in patients patient’s physician at higher than taking warfarin recommended doses

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Drug Side-effects (SEs) Mechanism of SE Contra-indications Interactions Alternatives

Opioids Commonly nausea, Binding to specific Patients already SSRIs, SNRIs-NERI, Non-opioid vomiting, drowsiness opioid receptors in on sedative and 5-HT-serotonin; analgesics alone & constipation CNS and GI tract hypnotic medication TCAs, MAOIs* or in combination Rarely dose- (eg benzodiazepines, with opioids dependent respiratory barbiturates) reduce dose- depression related SEs History of alcohol or other substance abuse represent a relative contra- indication

Abbreviations: PG, prostaglandins; SSRIs, selective serotonin re-uptake inhibitors; SNRIs, selective serotonin; NERI, norepinephrine re-uptake inhibitors; TCAs, tricyclic antidepressants; MAOIs, monoamine oxidase inhibitors.

*Opioids should not be administered within 14 days of MAOIs owing to potential for severe hypotension, CNS and respiratory effects. Concomitant administration may cause serotonin syndrome. All opioids should be used with caution in combination with CNS depressants owing to increased risk for respiratory depression and sedation. Table 4. Common side-effects of NSAIDs, paracetamol and opioids.

by interrupting ascending nociceptive comparisons between oral analgesics.29 from arachidonic acid in the arachidonic information or depressing interpretation of The results from this review and previous pathway (Figure 2). Prostaglandins are the information within the CNS. For dental systematic reviews of randomized post- involved in inflammation, nociception and or routine day case surgery post-surgical surgical trials helped to formulate fever modulation (prostaglandin E2 in the pain control, oral analgesia prescribed the Oxford League Table of Analgesics in hypothalamus). These peripheral events are usually over-the-counter (OTC) Acute Pain,30 which is used by healthcare are followed by a cascade of events in the analgesic medications including, NSAIDs, professions worldwide. Analgesic efficacy spinal cord within the set pain pathways paracetamol, opiates or combinations is expressed as the number-needed-to- associated with inflammatory pain involving of these medications. Their pharmaco- treat (NNT). This estimates the number of specific transmitters, receptors and mechanisms for pain reduction remain not patients who need to receive the analgesic mediators (Figure 3).31 fully understood but what little is known is for one to achieve at least 50% relief of pain NSAIDs are the gold standard illustrated in Figure 1. compared with a placebo over a six-hour analgesics in dentistry as acute post- Analgesics are classified as treatment period. The more effective the operative dental pain is inflammatory opioids or non-opioids and may act analgesic, the lower the NNT. The Bandolier in nature. Hence, they are superior to at different sites, depending on their NNT table shows that oral NSAIDs perform opioids.32 Ibuprofen 200/400 mg or mechanism of action. Non-steroidal anti- well, and that paracetamol in combination diclofenac 25/50 mg, three times daily, are inflammatory drugs (NSAIDs) decrease with an opioid is also effective. commonly prescribed NSAIDs. pain resulting from inflammatory reactions NSAIDS are broadly classified (arachidonic acid cascade). Opioids may NSAIDs as non-selective cyclo-oxygenase (COX) 1, affect emotional aspects of pain and can NSAIDs are known for their 2 enzyme inhibitors (ibuprofen, diclofenac, modify transmission of pain information in analgesic, antipyretic and anti-inflammatory ) or selective COX-2 enzyme the dorsal horn (descending modulation). properties. These therapeutic effects, inhibitors (celecoxib, rofecoxib). The non- Non-opioid analgesics (including as well their associated side-effects, are selective group is further subdivided based paracetamol and NSAIDs) have been mostly due to NSAID inhibition of the on its derivative compounds. demonstrated to be superior analgesics enzyme cyclo-oxygenase (COX) and NSAIDs are contra-indicated in dental pain compared to opioids at hence prostaglandin (PG) production. for patients who have a history of gastro- 27 conventional doses. Following trauma/surgery, arachidonic intestinal (GI) ulcer/erosions, anticoagulant A meta-analysis of Cochrane acid is released from phospholipid bilayers therapy/ bleeding disorders, nephropathy, reviews of randomized controlled trials in perturbed cell membranes by the or intolerance/allergy to such drugs. If (RCTs) testing the analgesic efficacy of NSAIDs are contra-indicated, paracetamol activated enzyme phospholipase A2. COX individual oral analgesics in acute post- enzyme then catalyses the formation may be used as an alternative (Table 4). operative pain has helped facilitate indirect of prostaglandins and thromboxane Pre-operative/preventive use

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for maximum benefit.32 Pre-operative ibuprofen has been shown to be more effective at reducing acute post- operative pain than paracetamol or paracetamol with , although the paracetamol was at suboptimal dose of 600 mg (as opposed to 1 g).33

Paracetamol Paracetamol is one of the most popular and widely used drugs for first-line treatment of fever and pain.34 Paracetamol does not demonstrate significant anti-inflammatory properties, implying a mode of action that differs from that of NSAIDs.29 Paracetamol is commonly prescribed as 1 g, four times daily. Overdose of paracetamol can cause hepatotoxicity and death from liver failure, so clear instructions on dose and timing should be given to patients.35 Figure 1. Where analgesics work. Although the efficacy of paracetamol is well established, its mode of action is still poorly understood. Paracetamol’s significant anti-pyrexial activity suggests that the drug acts centrally. The following five mechanisms have been suggested: 1. Inhibition of cyclo-oxygenase isoenzymes (COX1, 2,3); 2. Interaction with the serotoninergic inhibitory descending pathway; 3. The endogenous opioid pathway (primarily descending); 4. Increase in cannabinoid/vallinoid tone; and 5. Involvement in the nitric oxide pathway.36 A recent study at King’s College London demonstrated, in the rat, that spinal pain receptors TRPA1 have a crucial role in the antinociceptive effects of paracetamol.37 Peripheral TRPA1 did not demonstrate the same involvement.37 Paracetamol is a safe drug, which is well tolerated, with Figure 2. The arachidonic pathway. minimal side-effects. It is metabolized by the liver and is hepatotoxic. Hence caution is required in its use in chronic of NSAIDs has been demonstrated to Administering NSAIDs before surgery will alcoholic patients and those with liver decrease the intensity of post-operative inhibit prostaglandin synthesis and reduce damage (Table 4). A Cochrane review, pain and swelling.25,33 During surgery, the the post-operative pain experience once in 2007, of RCTs demonstrated that synthesis of prostaglandins at the surgical the local anaesthesia wears off. Optimum paracetamol is an effective drug to use site will transmit nociceptive impulses and serum levels of NSAID should be established for post-operative pain following oral 38 sensitize the nervous system to the pain. whilst the tissue remains anaesthetized surgery, with very few adverse effects.

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Figure 3. The cascade of events in the spinal cord associated with promotion and inhibition of inflammatory pain. Key Inflammatory agents regulate TRPA1 and TRPV1 through direct and indirect mechanisms. Tissue injury, ischaemia, or cellular stress generates an array of pro-algesic and pro-inflammatory agents, collectively referred to as the ‘inflammatory soup.’ This includes extracellular protons (H+), bradykinin (BK), and nerve growth factor (NGF), as well as reactive oxygen species (ROS) that convert polyunsaturated fatty acids into reactive carbonyl species, such as 4-hydroxy-trans-2-nonenal (HNE). Some factors, such as HNE and protons, activate TRPA1 or TRPV1 directly, while others, such as BK and NGF, modulate channel gating indirectly by binding to cognate receptors (BR and TRKA, respectively) to activate cellular signalling cascades, most notably those downstream of phospholipase C (PLC). Thus, TRPA1 and TRPV1 function as polymodal signal integrators capable of detecting chemically diverse products of cell and tissue injury. In doing so, these channels promote pain hypersensitivity by depolarizing the primary afferent nerve fibre and/or lowering thermal or mechanical activation threshold. (With permission from Nature Reviews Immunology).31

Opioids of medication is not the first choice for analgesic efficacy at lower doses and Opioids bind to specific opioid management of mild to moderate acute minimizing side-effects. It also advocates receptors in the central nervous system orofacial pain. regular administration of analgesics (every 4 (CNS), causing reduced pain perception to 6 hours) rather than ‘on demand’.39 and reaction to pain and increased pain Selecting analgesics according to WHO NSAIDs should be combined tolerance. In addition to these desirable analgesic ladder with paracetamol, when possible, as they analgesic effects, binding to receptors in An analgesic ladder, for differing provide greater analgesia than when used the CNS may cause adverse events, such pain severity, was introduced by the World alone,36 reducing the effective dose and, as drowsiness and respiratory depression. Health Organization in 1986 to assist hence, possible side-effects. This synergistic Moreover, binding to receptors elsewhere in analgesic prescribing by clinicians (Figure effect is attributed to different sites of the body (primarily the GI tract) commonly 4). Non-opioid analgesics (paracetamol and action of the two analgesics.32 Oral non- causes nausea, vomiting and constipation. NSAIDs) form the basis of managing mild steroidal drugs often supplement the initial In an effort to reduce the amount of pain with introduction of opioid analgesia prescription of paracetamol. The latter is opioid required for pain relief, and so if the pain worsens.39 This principle of used pro re nata (PRN – when necessary) reduce undesirable side-effects, opioids multi-modal analgesia highlights that the as the pain decreases. Taking paracetamol are commonly combined with non-opioid gold standard of pain management is by with NSAIDs only when necessary can limit analgesics. On this basis, the opioid group combinations of drugs, thereby maximizing potential side-effects of the NSAID.

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non-reversible. Intermittent sharp, shooting World Health Organization (WHO) are also symptomatic of trigeminal , so care must be taken not to Analgesic ladder label toothache mistakenly as neuralgia. Confirmation of the type of pulpitis is a clinical diagnosis. If the insult persists, the pulpitis will become irreversible with increased Opioid pulpal vascularity and resultant pressure, Moderate to severe pain Step 3 Tramadol inducing ischaemia and causing sensitivity to heat with prolonged pain. Once necrosis of the dental pulp has occurred, the infection Paracetamol spreads through the apex of the tooth into Mild to moderate pain Step 2 Diclofenac the surrounding bone and periodontal Opioid membrane, initiating periodontal Ibuprofen with Paracetamol or inflammation and eventually a dental Mild pain Step 1 Paracetamol alone if unable to take abscess causing spontaneous long-lasting

NSAIDs to persisting? Move Pain next level down Move of toxicity? Signs a level pain on biting on the tooth. Typically, the pain associated with an abscess is described Figure 4. Analgesic ladder, for differing pain severity, was introduced by the World Health Organization as spontaneous aching or throbbing and, if in 1986 to assist analgesic prescribing by clinicians. associated with swelling in the jaw, trismus or lymphadenopathy, it may be indicative of an acute spreading infection. Thus different stages of infection have different clinical Table 5 shows the authors’ disease (gum disease), the second most presentations (Figure 5). suggested analgesic regimen for acute common infection, is painless similar to trigeminal pain. other chronic mycobacteria infections, eg leprosy. Dentofacial pain is a common Management presentation in general practice: Protection of the pulp to Management of acute  In a carious tooth, pain that is site- bacterial infection and chemical irritation odontogenic pain specific, severe and spontaneous usually by dietary and salivary content must Odontogenic pain refers to pain denotes extension of caries into the tooth be undertaken promptly to minimize initiating from the teeth or their supporting pulp; persistence of acute pulpitis, thus evolving structures, the mucosa, gingivae, maxilla,  Caries does not always appear as a cavity into chronic irreversible pulpitis. This mandible or periodontal membrane. in the tooth, but may lie beneath intact treatment will involve a filling or restoration, enamel or on surfaces between teeth; which will resolve reversible pulpitis.  Examination of dental pain should Irreversible pulpitis may be managed Aetiology of acute orofacial include firm percussion (eg with a in acute episodes by pulpal extirpation, pain depressor). Tenderness on percussion tooth extraction with analgesia using Orofacial pain can be associated denotes progression of infection into the non-steroidal anti-inflammatory drugs with pathological conditions or disorders periapical tissues. (NSAIDs) if required. Routine prescription related to somatic and neurological A cross-sectional survey of antibiotics is unacceptable for the structures. There are a wide range of causes reported that a third of Brazilian management of acute dental pain and of acute orofacial pain conditions, the most schoolchildren reported toothache over a should be solely reserved where local causal common being dental pain. Toothache 6-month period. The major predictor of the removal (pulp extirpation or extraction or can be very difficult to diagnose and may prevalence and severity of pain was pattern inadequate drainage) has failed OR the refer to pain initiating from the pulp, of dental attendance (p<0.001).41 patient presents with a spreading infection peri-radicular tissues or non-odontogenic that cannot be immediately dealt with sources. Diagnosis and management by and requires referral to secondary care. dental practitioners is by thorough pain Dental pulpitis (‘toothache’) Antibiotic prescription should comply with history-taking, dental clinical examination, In healthy teeth, pain is often The Scottish Dental Clinical Effectiveness 42 and radiographs. due to dentine sensitivity on cold, sweet Programme (SDCEP). Toothache (see below) is or physical stimulus. Dental pulpitis may caused by inflammation of the dental pulp be due to infection from dental caries Exposed or dentine (Figure 5) as a result of dental caries, the close to the pulp, inflammation caused by There is tooth sensitivity from most common human infective disease chemical or thermal insult subsequent to cold fluids and/or air, a reflection of a worldwide.40 Interestingly, periodontal dental treatment, and may be reversible or healthy pulp. With , recent

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Recommended Alternative

Mild pain Ibuprofen 200/400 mg Paracetamol 1g QDS (eg routine restorative dental work, TDS Reduce to PRN routine extraction, routine endodontic treatment, scaling) Reduce to paracetamol 1g QDS then PRN

Moderate pain Ibuprofen 400/600 mg TDS + Paracetamol 1 g QDS + codeine 30 mg (eg surgical dental extractions, implant paracetamol 1 g QDS QDS surgery) Reduce to paracetamol 1 g QDS with Reduce to paracetamol 1 g QDS then PRN ibuprofen 400 mg PRN

Severe pain Ibuprofen 200/400 mg QDS + Paracetamol 1 g QDS + codeine 60 mg (eg osteotomies, open reduction internal paracetamol 1 g QDS + codeine 30 mg QDS fixation of jaws, autologous bone graft) Diclofenac 25/50 mg TDS + paracetamol Reduce to paracetamol 1 g QDS then PRN 1 g QDS + codeine 30 mg QDS Reduce to ibuprofen 400 mg + paracetamol 1 g QDS Reduce to paracetamol 1 g QDS with ibuprofen PRN

Abbreviations: TDS, 3 times/day; QDS, 4 times/day; PRN, as needed

Table 5. Suggested analgesic regimens for acute trigeminal pain.

scaling, or toothwear due to a high acid diet will develop a chronic neuropathic pain The Scottish Dental Clinical Effectiveness or gastric reflux, there may be generalized state (see section on persistent post-surgical Programme (SDCEP).42 Antibiotics may be dentine sensitivity. Management is trigeminal pain). prescribed if the infection persists after summarized in Table 6. endodontic therapy or Dental management for or adequate drainage of pus was not This is either therapy possible. Metronidazole (200 mg TDS PO Apical pain with removal of the necrotic pulp or tooth 3 days) and/or amoxycillin (250 mg QDS This can be caused by infection extraction. Periapical inflammation can PO 3 days) are the antibiotics of choice spreading through the of lead to a of the face characterized with review at 3 days. The analgesics of the tooth into the apical periodontal region by a rapid spread of bacteria and their choice for dental inflammatory pain are causing inflammation (apical periodontitis) breakdown products into the surrounding ibuprofen (4-600 mg Soluble QDS PO PRN) and ultimately a dental abscess if left tissues causing extensive oedema and combined simultaneously with paracetamol untreated. Iatrogenic apical pain may pain. If systemic signs of infection are (acetaminophen 500–1000 mg QDS PO result after dental treatment including present, for example fever and , PRN). Table 4 provides more information premature contact if a restoration is left as well as swelling and possibly trismus about contra-indications and side-effects of high in occlusion. This is characterized (limitation of mouth opening), this is a these medications. by an initial sharp pain, which becomes surgical emergency. Antibiotic treatment duller after a period. The pain is due to alone is not suitable or recommended. a recent tooth restoration that is ‘high’ If pus is present, it needs to be drained, compared with the normal occlusion when Pain commonly arises from the the cause eliminated, and host defences biting together and will persist until the supporting gingivae and mucosa when augmented with antibiotics. The microbial height is reduced. Apical pain may also be infection arises from bacterial infection spectrum is mainly gram positive, including induced post-endodontic treatment. This around an erupting tooth (teething or anaerobes. Appropriate antibiotics is severe aching pain following endodontic pericoronitis). Along with caries, it is one of are metronidazole with or without treatment such as root canal therapy or the most common causes for the removal amoxycillin. Other antibiotics, including 43 apicectomy and should be managed with of third molar teeth (wisdom teeth). The Augmentin, erythromycin and penicillin, analgesia similar to pulpitis; antibiotics are pain may be constant or intermittent, but are not recommended for dental infections. not recommended. While the majority of is often aggravated when biting down Antibiotic prescription should comply with patients improve over time (weeks), a few with opposing maxillary teeth. Where June 2015 DentalUpdate 455 OralSurgery

History Special investigations Management

Dentine sensitivity Short, sharp pain on stimulation Clinical exam exposed dentine Prevention of cause (eg No lingering pain brushing) instruction/ technique Desensitizing agents Primers, varnishes, sealants

Reversible pulpitis Pain on stimulation Sensitivity tests (EPT/ Replacement restoration +/- Short, sharp duration Endofrost/heat) lining X-rays – caries/leaking restorations

Irreversible pulpitis Pain on stimulation but also Sensitivity tests Root canal restoration/ may be spontaneous X-rays – caries/leaking restorations pulpotomy/ extraction Dull aching throbbing poorly localized pain May keep awake at night

Acute apical periodontitis May have pulpal symptoms Sensitivity tests negative Occlusal adjustment/ root (AAP) previously response canal treatment/extraction Recent treatment (trauma, Radiography (no radiolucency mechanical/chemical damage present) to PDL) Bite test Tooth tender to touch/ bite High restoration/parafunction Tooth may feel elevated in the socket Localized pain

Acute exacerbation of chronic May have history of pulpal Radiography / apical periodontitis symptoms and AAP in the past extraction Swelling, tenderness on mucosa, Tooth is TTP

Acute periapical abscess Tenderness on percussion/ Sensitivity tests Root canal restoration/ of tooth/mucosa X-rays – may have widened PDL extraction Tooth mobility Periapical pathology present Localized intra/extra-oral abscess when an exacerbation of chronic May feel unwell with raised apical periodontitis temperature

Pericoronitis Aching, localized swelling, +/- Sectional DPT Irrigation saline +/- facial swelling, trismus If high risk – cone beam CT +/- metronidazole 3 days

Alveolar osteitis Worsening pain 3/7 post- Irrigation saline +/- extraction, halitosis alvogyl

Cracked tooth Pain on biting/releasing – Bite on firm object – toothsleuth Cuspal coverage/ Root canal short duration Remove restoration & visualize treatment/ extraction May be history of pulpal with microscope +/- methylene symptoms blue

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History Special investigations Management

Premature contact Pain on biting Articulating paper – check for Adjustment/ replacement of heavy contact – eg recent tooth restoration restorations

Maxillary Rhinorrhoea, congestion, CBCT if unresponsive to treatment Antibiotics only if persistent > headache, pain on leaning 1 week or if very severe pyrexia forwards/over sinus, dental pain Decongestants Karvol Pseudo-ephedrine nasal spray/ drops Functional endoscopic sinus surgery

Temporomandibular Aching jaw joint, around ear – Tenderness Analgesics – ibuprofen/ joint disorder continuous/on chewing/opening Recent stress paracetamol wide Parafunction habits – night Limit mouth opening Limited mouth opening , chewing gum Soft diet Deviation mandible to affected Avoid parafunctional habits side +/- click/crepitus – Warm/cold compress

Abbreviations: PDL – periodontal ligament; EPT – electrical pulp test; TTP – tender to percussion *NB this list is not exhaustive – please refer to Hegarty & Zakrzewska 2011.7

Table 6. Summary of the common acute dental pain states and management.

possible, extraction is always preferable The Scottish Dental Clinical Effectiveness Necrotizing ulcerative (NUG) to medication. If the infection is acute and Programme (SDCEP).42 (formerly acute necrotizing ulcerative spreading and extraction is not possible gingivitis) immediately then antibiotics may be This is a rapidly progressive (dry socket) prescribed. Management is summarized in infection of the gingival tissues that causes This is a common complication Table 6. ulceration of the interdental gingival after extraction, especially mandibular papillae.48 It can lead to extensive destruction. 44 third molars with a reported incidence Young to middle-aged people with reduced Periodontitis ranging from 0.5 to 5% in routine resistance to infection are commonly affected with extractions to 1 to 37.5% in lower third (diabetes, HIV infection, chemotherapy). 45 gradual bone loss rarely causes pain and molar extractions. It is defined as Males are more likely to be affected than patients may be unaware of the disorder ‘postoperative pain inside and around the females, with stress, smoking and poor oral until tooth mobility is evident. There extraction site, which increases in severity hygiene being the predisposing factors. is quite often bleeding from the at any time between the first and third Halitosis, spontaneous gingival bleeding, and and sometimes an unpleasant taste. day after the extraction, accompanied by a `punched-out’ appearance of the interdental This is usually a generalized condition, a partial or total disintegrated blood clot papillae are all important signs.49 Patients however, deep pocketing with extreme within the alveolar socket with or without mainly complain of severe gingival tenderness 46 bone loss can occur around isolated halitosis’. The pain is likely to be caused with pain on eating and toothbrushing. The teeth. Food impaction interproximally, by irritation of the nerve endings in the pain is dull, deep-seated and constant. The caused by an overhang of a restoration exposed bone by necrotic food and debris gums can bleed spontaneously and there is or poor interproximal tooth contact, can trapped in the socket. Patients should be also an unpleasant taste in the mouth and cause localized gingival inflammation routinely warned of a possible dry socket obvious halitosis. Oral hygiene instruction, 47 and pain. Aggressive prior to teeth extractions. Irrigation of , and requires removal of local and systemic the socket (avoid chlorhexidine containing metronidazole are the treatment regimen contributory factors, where possible, and irrigates due to recent reports of of choice. Antibiotic prescription should adjunctive periodontal deep cleaning anaphylaxis) and placement of a sedative comply with The Scottish Dental Clinical and scaling. Antibiotics are not indicated dressing (Alvogyl) is the treatment of Effectiveness Programme (SDCEP).42 The for periodontal disease management. choice. Management is summarized in analgesics of choice for dental inflammatory Antibiotic prescription should comply with Table 6. June 2015 DentalUpdate 457 OralSurgery

a

d

b

e

c

Figure 5. (a) Dental pulpal pain characteristics. (b) Types of ‘dental’ pain. (c) Dental pulpal pain theory: Activation theory. (d) Dental pulpal pain theory: Transduction theory. (e) Dental pulpal pain theory: Hydrodynamic theory.

June 2015 DentalUpdate 459 OralSurgery

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