Pain part 3: acute orofacial pain

Pain assessment

The clinician is beholden to take a full and comprehensive history to build trust and understanding of the patient and his/her complaint. Acute pain will have onset in the last days/weeks and generally has been present for less than 3 months. The pain may be associated with key inflammatory signs (tumor, dolor, calor, rubor and loss of function) but if caused by a ‘cold bacteria’ may not have the traditional inflammatory signs (eg dry socket). Acute pain is inflammatory pain responding to anti-inflammatories (eg paracetamol and NSAIDs) and antibiotics, if related to an infective cause.

There is no absolute measure of pain as it is a purely subjective experience. However, pain assessment is essential in diagnosing and monitoring a patient's response to treatment. Pain rating scales are often used in assessing pain intensity. They are quick and easy to use (Table 2),8 whereas pain questionnaires can often assess the quality and character of the pain (eg McGill Pain Questionnaire (MPQ)), as well as its intensity.9 The MPQ consists primarily of three major classes of word descriptors; sensory, affective and evaluative to specify the pain experience.8

Management of intra-operative pain

Local anaesthesia (LA) is fundamental for pain control in outpatient oral surgery and dental procedures. Local anaesthetic is defined as a drug which reversibly prevents transmission of the nerve impulse in the region to which it is applied, without affecting consciousness.10 It is frequently used to control intra-operative and immediate post-operative pain. During acute tissue trauma mediated pain (eg tooth extraction), local anaesthetic blocks the pain signal transmission to the cerebral cortex, preventing pain perception and processing. Hence, local anaesthetic should always be used, even if the patient is under general anaesthesia, as it prevents nervous system sensitization and, hence, reduces post-operative pain.11

Local anaesthetic agents bind to sodium channels on axons, thus inhibiting the rapid passage of sodium ions and propagation of an action potential. There are two theories of the mechanisms of action of local anaesthetic both of which involve perturbation of the nerve cell's sodium channels and, hence, prevention of nerve depolarization and firing. The membrane expansion theory suggests non-specific swelling of the cell membrane by absorption of the LA, whilst the newer specific binding theory describes binding of LA to a specific binding site of the sodium channel. Discovery of specific drug binding sites allows for the possibility of developing anaesthetics with greater sensitivity for specific sodium channels with reduced side-effects.12

Lidocaine is the most commonly administered local anaesthetic by dental practitioners, although other available solutions (prilocaine, mepivacaine and articaine) offer advantages in certain situations (Table 3). In the severely medically-compromised patient, such as those with unstable angina, an adrenaline-free solution such as 3% prilocaine with felypressin should be used.13 In a meta-analysis, articaine 4% was found to be superior to lidocaine 2% in anaesthetizing lower first molars.14

Although there are limited scientific studies in which local anaesthetics with higher concentrations (4%) result in higher incidence of paraesthesia,15 there remains a trend to avoid articaine 4% use in inferior alveolar nerve (IAN) blocks. Local anaesthetic related lingual nerve injury is most likely to occur when multiple inferior alveolar nerve blocks are given, regardless of the local anaesthetic agent used.16 Importantly, buccal infiltration articaine will most likely avoid inferior dental blocks with lidocaine for most of dentistry, also reducing the likelihood of IAN LA-related injuries.

Studies have suggested benefit in using bupivacaine (Marcaine), a long-acting local anaesthetic, to limit post-operative pain following third molar surgery17^,18 and endodontic treatment.19 Reports range from a reduction in pain at 8 hours18 to 7 days17 post-operatively. It is important to note that bupivacaine exhibits this property only when used as a nerve block and not when used as an infiltration. Levobupivacaine is a newer anaesthetic solution with an improved safety profile than, and equivalent efficacy to, bupivacaine (the latter has rare reports of causing severe central nervous system (CNS) and cardiovascular adverse effects).20 A double blind study showed similar anaesthetic efficacy between bupivacaine (0.5%) and levobupivacaine (0.5%) in inferior alveolar nerve blocks, suggesting that levobupivacaine is a useful alternative to bupivacaine owing to its lower toxicity.21

Post-surgical pain management

Effective post-operative pain management is fundamental to quality dental care, and is likely to speed recovery. Conventional analgesics act by interrupting ascending nociceptive information or depressing interpretation of the information within the CNS. For dental or routine day case surgery post-surgical pain control, oral analgesia prescribed are usually over-the-counter (OTC) analgesic medications including, NSAIDs, paracetamol, opiates or combinations of these medications. Their pharmaco-mechanisms for pain reduction remain not fully understood but what little is known is illustrated in Figure 1.

Analgesics are classified as opioids or non-opioids and may act at different sites, depending on their mechanism of action. Non-steroidal anti-inflammatory drugs (NSAIDs) decrease pain resulting from inflammatory reactions (arachidonic acid cascade). Opioids may affect emotional aspects of pain and can modify transmission of pain information in the dorsal horn (descending modulation). Non-opioid analgesics (including paracetamol and NSAIDs) have been demonstrated to be superior analgesics in dental pain compared to opioids at conventional doses.27

A meta-analysis of Cochrane reviews of randomized controlled trials (RCTs) testing the analgesic efficacy of individual oral analgesics in acute post-operative pain has helped facilitate indirect comparisons between oral analgesics.29 The results from this review and previous systematic reviews of randomized post-surgical analgesic trials helped to formulate the Oxford League Table of Analgesics in Acute Pain,30 which is used by healthcare professions worldwide. Analgesic efficacy is expressed as the number-needed-to-treat (NNT). This estimates the number of patients who need to receive the analgesic for one to achieve at least 50% relief of pain compared with a placebo over a six-hour treatment period. The more effective the analgesic, the lower the NNT. The Bandolier NNT table shows that oral NSAIDs perform well, and that paracetamol in combination with an opioid is also effective.

NSAIDs

NSAIDs are known for their analgesic, antipyretic and anti-inflammatory properties. These therapeutic effects, as well their associated side-effects, are mostly due to NSAID inhibition of the enzyme cyclo-oxygenase (COX) and hence prostaglandin (PG) production. Following trauma/surgery, arachidonic acid is released from phospholipid bilayers in perturbed cell membranes by the activated enzyme phospholipase A₂. COX enzyme then catalyses the formation of prostaglandins and thromboxane from arachidonic acid in the arachidonic pathway (Figure 2). Prostaglandins are involved in inflammation, nociception and fever modulation (prostaglandin E2 in the hypothalamus). These peripheral events are followed by a cascade of events in the spinal cord within the set pain pathways associated with inflammatory pain involving specific transmitters, receptors and mediators (Figure 3).31

NSAIDs are the gold standard analgesics in dentistry as acute post-operative dental pain is inflammatory in nature. Hence, they are superior to opioids.32 Ibuprofen 200/400 mg or diclofenac 25/50 mg, three times daily, are commonly prescribed NSAIDs.

NSAIDS are broadly classified as non-selective cyclo-oxygenase (COX) 1, 2 enzyme inhibitors (ibuprofen, diclofenac, aspirin) or selective COX-2 enzyme inhibitors (celecoxib, rofecoxib). The non-selective group is further subdivided based on its derivative compounds.

NSAIDs are contra-indicated for patients who have a history of gastro-intestinal (GI) ulcer/erosions, anticoagulant therapy/bleeding disorders, nephropathy, or intolerance/allergy to such drugs. If NSAIDs are contra-indicated, paracetamol may be used as an alternative (Table 4).

Table 4. Common side-effects of NSAIDs, paracetamol and opioids.

Drug	Side-effects (SEs)	Mechanism of SE	Contra-indications	Interactions	Alternatives
NSAIDs (eg ibuprofen 400 mg, diclofenac 50 mg)	GI bleeding	Erosion of stomach & intestine due to reduced production of protective mucous lining stimulated by PG. Systemic & direct mucosal contact effect	History gastric ulcer/gastro-oesophageal reflux disease (GORD)	Anticoagulants (warfarin, clopidogrel), SSRIs	Paracetamol opioids
	Prolonged bleeding	Reduced thromboxane A2 reduces platelet aggregation	Patients with bleeding disorders or on anticoagulant therapy, especially the elderly, have increased risk of severe GI bleed	Anticoagulant therapy (warfarin, clopidogrel) can increase INR	Paracetamol opioids
	Nephrotoxicity	Reduced renal function due to reduced PG production which is necessary for renal perfusion	Patients with compromised renal function		Paracetamol opioids
	Aspirin/NSAID intolerance or allergy	Inhibition of COX shunts arachidonic pathway toward leukotriene synthesis – signs and symptoms allergic response eg bronchospasm & anaphylaxis	Individuals sensitive to subtle elevation in leukotrienes – usually asthmatics Patients allergic to NSAIDs		Paracetamol opioids
			PGs maintain patency of the ductus arteriosus during foetal development, especially 3rd trimester – avoid in pregnancy		Paracetamol
				Lithium and methotrexate serum levels elevated during concurrent NSAID use	Paracetamol opioids
Paracetamol	Liver & kidney damage when taken at higher than recommended doses	Overdose – can result in hepatotoxicity	Hepatic impairment chronic alcoholism	Increased INR may occur in patients taking warfarin	Check with patient's physician
Opioids	Commonly nausea, vomiting, drowsiness & constipationRarely dose-dependent respiratory depression	Binding to specific opioid receptors in CNS and GI tract	Patients already on sedative and hypnotic medication (eg benzodiazepines, barbiturates)History of alcohol or other substance abuse represent a relative contra-indication	SSRIs, SNRIs-NERI, 5-HT-serotonin; TCAs, MAOIs*	Non-opioid analgesics alone or in combination with opioids reduce dose-related SEs

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.

Pre-operative/preventive use of NSAIDs has been demonstrated to decrease the intensity of post-operative pain and swelling.25^,33 During surgery, the synthesis of prostaglandins at the surgical site will transmit nociceptive impulses and sensitize the nervous system to the pain. Administering NSAIDs before surgery will inhibit prostaglandin synthesis and reduce the post-operative pain experience once the local anaesthesia wears off. Optimum serum levels of NSAID should be established whilst the tissue remains anaesthetized 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 codeine, although the paracetamol was at suboptimal dose of 600 mg (as opposed to 1 g).33

Selecting analgesics according to WHO analgesic ladder

An analgesic ladder, for differing pain severity, was introduced by the World Health Organization in 1986 to assist analgesic prescribing by clinicians (Figure 4). Non-opioid analgesics (paracetamol and NSAIDs) form the basis of managing mild pain with introduction of opioid analgesia if the pain worsens.39 This principle of multi-modal analgesia highlights that the gold standard of pain management is by combinations of drugs, thereby maximizing analgesic efficacy at lower doses and minimizing side-effects. It also advocates regular administration of analgesics (every 4 to 6 hours) rather than ‘on demand’.39

NSAIDs should be combined with paracetamol, when possible, as they provide greater analgesia than when used alone,36 reducing the effective dose and, hence, possible side-effects. This synergistic effect is attributed to different sites of action of the two analgesics.32 Oral non-steroidal drugs often supplement the initial prescription of paracetamol. The latter is used pro re nata (PRN – when necessary) as the pain decreases. Taking paracetamol with NSAIDs only when necessary can limit potential side-effects of the NSAID.

Table 5 shows the authors' suggested analgesic regimen for acute trigeminal pain.

Table 5. Suggested analgesic regimens for acute trigeminal pain.

	Recommended	Alternative
Mild pain (eg routine restorative dental work, routine extraction, routine endodontic treatment, scaling)	Ibuprofen 200/400 mg TDSReduce to paracetamol 1g QDS then PRN	Paracetamol 1g QDSReduce to PRN
Moderate pain (eg surgical dental extractions, implant surgery)	Ibuprofen 400/600 mg TDS + paracetamol 1 g QDSReduce to paracetamol 1 g QDS with ibuprofen 400 mg PRN	Paracetamol 1 g QDS + codeine 30 mg QDSReduce to paracetamol 1 g QDS then PRN
Severe pain (eg osteotomies, open reduction internal fixation of jaws, autologous bone graft)	Ibuprofen 200/400 mg QDS + Paracetamol 1 g QDS + codeine 30 mgDiclofenac 25/50 mg TDS + paracetamol 1 g QDS + codeine 30 mg QDSReduce to ibuprofen 400 mg + paracetamol 1 g QDSReduce to paracetamol 1 g QDS with ibuprofen PRN	Paracetamol 1 g QDS + codeine 60 mg QDSReduce to paracetamol 1 g QDS then PRN

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

Management

Protection of the pulp to bacterial infection and chemical irritation by dietary and salivary content must be undertaken promptly to minimize persistence of acute pulpitis, thus evolving into chronic irreversible pulpitis. This treatment will involve a filling or restoration, which will resolve reversible pulpitis. Irreversible pulpitis may be managed in acute episodes by pulpal extirpation, tooth extraction with analgesia using non-steroidal anti-inflammatory drugs (NSAIDs) if required. Routine prescription of antibiotics is unacceptable for the management of acute dental pain and should be solely reserved where local causal removal (pulp extirpation or extraction or inadequate pus drainage) has failed OR the patient presents with a spreading infection that cannot be immediately dealt with and requires referral to secondary care. Antibiotic prescription should comply with The Scottish Dental Clinical Effectiveness Programme (SDCEP).42

Exposed cementum or dentine

There is tooth sensitivity from cold fluids and/or air, a reflection of a healthy pulp. With gingival recession, recent scaling, or toothwear due to a high acid diet or gastric reflux, there may be generalized dentine sensitivity. Management is summarized in Table 6.

Apical pain

This can be caused by infection spreading through the apical foramen of the tooth into the apical periodontal region causing inflammation (apical periodontitis) and ultimately a dental abscess if left untreated. Iatrogenic apical pain may result after dental treatment including premature contact if a restoration is left high in occlusion. This is characterized by an initial sharp pain, which becomes duller after a period. The pain is due to a recent tooth restoration that is ‘high’ compared with the normal occlusion when biting together and will persist until the height is reduced. Apical pain may also be induced post-endodontic treatment. This is severe aching pain following endodontic treatment such as root canal therapy or apicectomy and should be managed with analgesia similar to pulpitis; antibiotics are not recommended. While the majority of patients improve over time (weeks), a few will develop a chronic neuropathic pain state (see section on persistent post-surgical trigeminal pain).

Dental management for dental abscess

This is either root canal therapy with removal of the necrotic pulp or tooth extraction. Periapical inflammation can lead to a cellulitis of the face characterized by a rapid spread of bacteria and their breakdown products into the surrounding tissues causing extensive oedema and pain. If systemic signs of infection are present, for example fever and malaise, as well as swelling and possibly trismus (limitation of mouth opening), this is a surgical emergency. Antibiotic treatment alone is not suitable or drecommended. If pus is present, it needs to be drained, the cause eliminated, and host defences augmented with antibiotics. The microbial spectrum is mainly gram positive, including anaerobes. Appropriate antibiotics are metronidazole with or without amoxycillin. Other antibiotics, including Augmentin, erythromycin and penicillin, are not recommended for dental infections. Antibiotic prescription should comply with The Scottish Dental Clinical Effectiveness Programme (SDCEP).42 Antibiotics may be prescribed if the infection persists after endodontic therapy or dental extraction or adequate drainage of pus was not possible. Metronidazole (200 mg TDS PO 3 days) and/or amoxycillin (250 mg QDS PO 3 days) are the antibiotics of choice with review at 3 days. The analgesics of choice for dental inflammatory pain are ibuprofen (4-600 mg Soluble QDS PO PRN) combined simultaneously with paracetamol (acetaminophen 500–1000 mg QDS PO PRN). Table 4 provides more information about contra-indications and side-effects of these medications.

Pericoronitis

Pain commonly arises from the supporting gingivae and mucosa when infection arises from bacterial infection around an erupting tooth (teething or pericoronitis). Along with caries, it is one of the most common causes for the removal of third molar teeth (wisdom teeth).43 The pain may be constant or intermittent, but is often aggravated when biting down with opposing maxillary teeth. Where possible, extraction is always preferable to medication. If the infection is acute and spreading and extraction is not possible immediately then antibiotics may be prescribed. Management is summarized in Table 6.

Periodontitis

Chronic periodontitis with gradual bone loss rarely causes pain and patients may be unaware of the disorder until tooth mobility is evident. There is quite often bleeding from the gums and sometimes an unpleasant taste. This is usually a generalized condition, however, deep pocketing with extreme bone loss can occur around isolated teeth. Food impaction interproximally, caused by an overhang of a restoration or poor interproximal tooth contact, can cause localized gingival inflammation and pain. Aggressive periodontal disease requires removal of local and systemic contributory factors, where possible, and adjunctive periodontal deep cleaning and scaling. Antibiotics are not indicated for periodontal disease management. Antibiotic prescription should comply with The Scottish Dental Clinical Effectiveness Programme (SDCEP).42

Alveolar osteitis (dry socket)

This is a common complication after extraction, especially mandibular third molars44 with a reported incidence ranging from 0.5 to 5% in routine extractions to 1 to 37.5% in lower third molar extractions.45 It is defined as ‘postoperative pain inside and around the extraction site, which increases in severity at any time between the first and third day after the extraction, accompanied by a partial or total disintegrated blood clot within the alveolar socket with or without halitosis’.46 The pain is likely to be caused by irritation of the nerve endings in the exposed bone by necrotic food and debris trapped in the socket. Patients should be routinely warned of a possible dry socket prior to teeth extractions.47 Irrigation of the socket (avoid chlorhexidine containing irrigates due to recent reports of anaphylaxis) and placement of a sedative dressing (Alvogyl) is the treatment of choice. Management is summarized in Table 6.

Necrotizing ulcerative gingivitis (NUG) (formerly acute necrotizing ulcerative gingivitis)

This is a rapidly progressive infection of the gingival tissues that causes ulceration of the interdental gingival papillae.48 It can lead to extensive destruction. Young to middle-aged people with reduced resistance to infection are commonly affected (diabetes, HIV infection, chemotherapy). Males are more likely to be affected than females, with stress, smoking and poor oral hygiene being the predisposing factors. Halitosis, spontaneous gingival bleeding, and a ‘punched-out’ appearance of the interdental papillae are all important signs.49 Patients mainly complain of severe gingival tenderness with pain on eating and toothbrushing. The pain is dull, deep-seated and constant. The gums can bleed spontaneously and there is also an unpleasant taste in the mouth and obvious halitosis. Oral hygiene instruction, debridement, hydrogen peroxide and metronidazole are the treatment regimen of choice. Antibiotic prescription should comply with The Scottish Dental Clinical Effectiveness Programme (SDCEP).42 The analgesics of choice for dental inflammatory pain are ibuprofen (400–600 mg soluble 3-4 times daily) combined simultaneously with paracetamol (500-1000 mg 4 times daily).50Table 4 provides more information about contra-indications and side-effects of these medications.

Maxillary sinusitis

Maxillary sinusitis often ‘mimics’ odontogenic pain and symptoms of pain forming inflammatory sinus disease, usually occur one week following an upper respiratory tract infection.51 The pain may be localized over the sinuses or it may mimic toothache in the maxillary posterior teeth. The pain tends to be increased on lying down or bending over. There is often a feeling of ‘fullness’ on the affected side. Acute sinusitis is usually viral in origin with treatment focused on relief of symptoms by using topical decongestants (<7 days) and saline irrigation, which help sinus drainage.51 If the patient is systemically unwell, feverish or there is evidence of spread of infection beyond the sinuses, then antibiotics should be prescribed.51 Referral to an ENT or otorhinolaryngologist specialist for endoscopic sinus surgery may be indicated in chronic cases.51 Routine prescription of antibiotics is unacceptable for the management of acute sinusitis. If persistent and appropriately confirmed by examination, necessary antibiotic prescription should comply with The Scottish Dental Clinical Effectiveness Programme (SDCEP).42

The most common viral infections include herpes simplex Types I and II and herpes zoster. Antiviral prescription for these cases should comply with The Scottish Dental Clinical Effectiveness Programme (SDCEP).42

Persistent pain may also involve neuropathic or neurovascular components, thus knowledge of the complexity of pain and local anatomy are crucial. This will enable the practitioner to diagnose and treat odontogenic causes, whilst simultaneously excluding sinister causes of pain requiring urgent management or neuropathic pain in which patients will not benefit from surgical or dental treatment.