Gnauck M, Magnusson T, Ekberg E. Knowledge and competence in temporomandibular disorders among Swedish general dental practitioners and dental hygienists. Acta Odontol Scand. 2017; 75:429-436
Durham J, Exley C, Wassell R, Steele J. ‘Management is a black art’–professional ideologies with respect to temporomandibular disorders. Br Dent J. 2007; 202
Cairns B. Pathophysiology of TMD pain–basic mechanisms and their implications for pharmacotherapy. J Oral Rehabil. 2010; 37:391-410
Goetz CG. Textbook of Clinical Neurology.Philadelphia, USA: Elsevier Health Sciences; 2007
Tanaka E, Detamore MS, Mercuri LG. Degenerative disorders of the temporomandibular joint: etiology, diagnosis, and treatment. J Dent Res. 2008; 87:296-307 https://doi.org/10.1177/154405910808700406
Louca Jounger S, Christidis N, Svensson P Increased levels of intramuscular cytokines in patients with jaw muscle pain. J Headache Pain. 2017; 18 https://doi.org/10.1186/s10194-017-0737-y
Shah JP, Thaker N, Heimur J Myofascial trigger points then and now: a historical and scientific perspective. PM R. 2015; 7:746-761
Feizerfan A, Sheh G. Transition from acute to chronic pain. Continuing Education in Anaesthesia, Critical Care & Pain. 2015; 15:98-102
Severeijns R, Vlaeyen JW, van den Hout MA, Weber WE. Pain catastrophizing predicts pain intensity, disability, and psychological distress independent of the level of physical impairment. Clin J Pain. 2001; 17:165-172 https://doi.org/10.1097/00002508-200106000-00009
Gatchel RJ, Peng YB, Peters ML The biopsychosocial approach to chronic pain: scientific advances and future directions. Psychol Bull. 2007; 133:581-624 https://doi.org/10.1037/0033-2909.133.4.581
Nackley AG, Tan KS, Fecho K Catechol-O-methyltransferase inhibition increases pain sensitivity through activation of both β2-and β3-adrenergic receptors. Pain. 2007; 128:199-208
Jiao K, Niu LN, Li QH beta2-Adrenergic signal transduction plays a detrimental role in subchondral bone loss of temporomandibular joint in osteoarthritis. Sci Rep. 2015; 5 https://doi.org/10.1038/srep12593
Küchler EC, Meger MN, Ayumi Omori M Association between oestrogen receptors and female temporomandibular disorders. Acta Odontol Scand. 2019; 78:181-188
Moore RA, Derry S, Wiffen PJ Overview review: comparative efficacy of oral ibuprofen and paracetamol (acetaminophen) across acute and chronic pain conditions. Eur J Pain. 2015; 19:1213-1223 https://doi.org/10.1002/ejp.649
Vaughan C, Ingram S, Connor M, Christie M. How opioids inhibit GABA-mediated neurotransmission. Nature. 1997; 390:611-614
Bouloux G. Use of opioids in long-term management of temporomandibular joint dysfunction. J Oral Maxillofac Surg. 2011; 69:1885-1891
Dionne RA. Pharmacologic treatments for temporomandibular disorders. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1997; 83:134-142 https://doi.org/10.1016/s1079-2104(97)90104-9
Silva R, Gerloni V, Connelly T. Medical Management of TMD.Cham, Switzerland: Springer; 2019
Mujakperuo HR, Watson M, Morrison R, Macfarlane TV. Pharmacological interventions for pain in patients with temporomandibular disorders. Cochrane Database Syst Rev. 2010; https://doi.org/10.1002/14651858.CD004715.pub2
Kulkarni S, Thambar S, Arora H. Evaluating the effectiveness of nonsteroidal anti-inflammatory drug(s) for relief of pain associated with temporomandibular joint disorders: A systematic review. Clin Exp Dent Res. 2020; 6:134-146 https://doi.org/10.1002/cre2.241
Senye M, Mir CF, Morton S, Thie NM. Topical nonsteroidal anti-inflammatory medications for treatment of temporomandibular joint degenerative pain: a systematic review. J Orofac Pain. 2012; 26:26-32
Singer E, Dionne R. A controlled evaluation of ibuprofen and diazepam for chronic orofacial muscle pain. J Orofac Pain. 1997; 11:139-146
Ta LE, Dionne RA. Treatment of painful temporomandibular joints with a cyclooxygenase-2 inhibitor: a randomized placebo-controlled comparison of celecoxib to naproxen. Pain. 2004; 111:13-21 https://doi.org/10.1016/j.pain.2004.04.029
Dong X-D, Svensson P, Cairns B. The analgesic action of topical diclofenac may be mediated through peripheral NMDA receptor antagonism. Pain. 2009; 147:36-45
Oluwajana F, Clarke P, Foster-Thomas E Temporomandibular disorders. Part 1: anatomy, aetiology, diagnosis and classification. Dent Update. 2022; 49:320-328
Foster-Thomas E, James M, Crawford C Temporomandibular disorders. Part 2: non-surgical management. Dent Update. 2022; 49:380-386
de Alencar Júnior F, Sabino V, Patricia G Patient education and self-care for the management of jaw pain upon awakening: a randomized controlled clinical trial comparing the effectiveness of adding pharmacologic treatment with cyclobenzaprine or tizanidine. J Oral Facial Pain Headache. 2014; 28:119-127
Häggman-Henrikson B, Alstergren P, Davidson T Pharmacological treatment of oro-facial pain–health technology assessment including a systematic review with network meta-analysis. J Oral Rehabil. 2017; 44:800-826
Ouanounou A, Goldberg M, Haas DA. Pharmacotherapy in temporomandibular disorders: a review. J Can Dent Assoc. 2017; 83
James M, Clarke P, Darcey R. Body dysmorphic disorder and facial aesthetic treatments in dental practice. Br Dent J. 2019; 227:929-933 https://doi.org/10.1038/s41415-019-0901-7
Awan KH, Patil S, Alamir AWH Botulinum toxin in the management of myofascial pain associated with temporomandibular dysfunction. J Oral Pathol Med. 2019; 48:192-200 https://doi.org/10.1111/jop.12822
Dutt S, Ramnani P, Thakur D, Pandit M. Botulinum toxin in the treatment of muscle specificoro-facial pain: a literature review. J Oral Maxillofac Surg. 2015; 14:171-175
Yurttutan M, Sancak K, Tüzüner A. Which treatment is effective for bruxism: occlusal splints or botulinum toxin?. J Oral Maxillofac Surg. 2019; 77:2431-2438
Abboud W, Hassin-Baer S, Joachim M Localized myofascial pain responds better than referring myofascial pain to botulinum toxin injections. Int J Oral Maxillofac Surg. 2017; 46:1417-1423
Cascos-Romero J, Vázquez Delgado E, Vázquez Rodríguez E, Gay Escoda C. The use of tricyclic antidepressants in the treatment of temporomandibular joint disorders: systematic review of the literature of the last 20 years. Med Oral Patol Oral Cir Bucal. 2009; 14:3-7
Rizzatti-Barbosa CM, Nogueira MT, de Andrade ED Clinical evaluation of amitriptyline for the control of chronic pain caused by temporomandibular joint disorders. Cranio. 2003; 21:221-225 https://doi.org/10.1080/08869634.2003.11746254
Kimos P, Biggs C, Mah J Analgesic action of gabapentin on chronic pain in the masticatory muscles: a randomized controlled trial. Pain. 2007; 127:151-160 https://doi.org/10.1016/j.pain.2006.08.028
Kukkar A, Bali A, Singh N, Jaggi AS. Implications and mechanism of action of gabapentin in neuropathic pain. Arch Pharm Res. 2013; 36:237-251 https://doi.org/10.1007/s12272-013-0057-y
Tchivileva IE, Hadgraft H, Lim PF Efficacy and safety of propranolol for treatment of temporomandibular disorder pain: a randomized, placebo-controlled clinical trial. Pain. 2020; 161:1755-1767 https://doi.org/10.1097/j.pain.0000000000001882
Temporomandibular disorders. Part 3: pain and pharmacological therapy Peter Clarke Funmi Oluwajana Martin James Charles Crawford Emma Foster-Thomas Rigel Allan Dental Update 2024 49:6, 707-709.
Authors
PeterClarke
DCT in Restorative Dentistry, Liverpool University School of Dentistry, Pembroke Place, Liverpool L3 5PS, UK (pete.t.clarke@gmail.com)
Temporomandibular disorders (TMD) comprise a variety of diagnoses with multifactorial aetiologies. The treatment of these conditions is often multimodal, reflecting the complex nature of their pathogenesis. Pharmacology has long been used for the control of inflammation and pain in various acute and chronic conditions. Although not the mainstay of treatment in TMD, pharmacology frequently plays a supportive role, and numerous drugs are available that act on several potential targets. This article, the third in a series of six, summarizes the pathogenesis of pain relevant to TMD, before reviewing the current medications available, their efficacy and their potential indications.
CPD/Clinical Relevance: Understanding the potential medications available can help clinicians select an appropriate drug to complement other treatment for TMD.
Article
Reversible treatments are recommended as first-line management for temporomandibular disorders (TMD).1 Pharmacological therapy is predominantly encompassed in reversible treatment; however, medications with considerable side effects are not deemed conservative options. Furthermore, many of the drugs used in the management of TMDs are off-license, with notable adverse reactions, leading them to be considered second-line treatments.1
Although varying by locality, medication is used relatively infrequently in the management of TMD.2 This can mainly be explained by inconclusive evidence, clinicians' self-reported lack of knowledge and the tendency for practitioners to use familiar therapies.2,3 Additionally, many of the recommended medications are not available in the UK's Dental Practitioners Formulary.4
The aim of this article is to explore the theories and indications behind pharmacological management relating to TMD. Prior to exploring the medications available, it is important to understand the pathophysiology of pain; first, to identify an appropriate therapeutic target, and secondly, to ensure congruity with the drug's mode of action, otherwise limited benefit can be anticipated.
Mechanisms of pain in TMD
Pain in TMD is predominantly of a muscular or joint origin. The mechanisms are still incompletely understood; however, commonality exists in the nociceptive neural pathways of both origins, even though local pathology varies (Figure 1). Reviews on this complex subject provide further details.5,6
Figure 1. Summary of the ascending nociceptive pathways of the trigeminal nerve. (NB the third order neurones demonstrate an interpretation of the complex multi-pathway synapses within the cortex). Descending pathways (not pictured) exist, originating from the cortex, that moderate pain perception at a higher level.
Pathophysiology of arthrogenic pain
The multiple sensory nerve endings of the temporomandibular joint (TMJ) can be stimulated by a variety of nociceptive stimuli. Mechanoreceptors in and around the joint can be stimulated by extremes of movements, joint overloading or from functional loading in maladaptive joint systems – all leading to pain.5 In more advanced disease, degeneration of joint components can occur. Mechanisms of degeneration are postulated to result from mechanical stress, either directly from macro/micro trauma, or indirectly from hypoxic perfusion injury or neurogenic inflammation.7 Ultimately, this leads to a cascade of downstream cytokine and neuropeptide release that results in hard and soft tissue damage, inflammation and pain perception.5,7
Pathophysiology of myofascial pain
In muscles diagnosed with myofascial pain, although limited gross pathological changes are seen,5 subclinical changes of increased inflammatory markers are present.8 The existence of ‘trigger zones’ is discussed in the literature concerning myofascial pain of the wider musculoskeletal system;9 whether or not they exist in TMD is unclear. Macroscopically, they are proposed to represent small clusters of hyperirritable muscle fibres known as ‘contraction knots’.9 It is hypothesized that sustained low-level contractions lead to selective recruitment of muscle fibres predisposing them to muscle damage – the so called ‘Cinderella theory’ (like Cinderella, they are always working).9 Alternative pain theories for myofascial pain are the ‘vicious cycle theory’, which suggests persistent pain leads to muscle hyperactivity and thus a negative feedback loop, or the ‘pain adaptation model’, which proposes muscle activity is altered to limit and prevent further damage. The former of these two is not generally accepted.5 Ultimately sustained contractions can cause muscle injury through ischaemia and hypoxia. Subsequent release of inflammatory and nociceptive mediators result in local and referred pain.5,8,9
Pain modulation: sensitization and genetics
Physiologically, it is known that pain perception can be altered both positively and negatively at peripheral and central levels. During the acute phase, a wide variety of inflammatory mediators are released at the site of tissue injury activating dormant c-fibres and lowering the activation threshold of neurone action potentials. This sustained state of hyperalgesia is termed ‘peripheral sensitization’ where future nociceptive stimuli may lead to prolonged and more diffuse pain perception.5,10 During the transition to chronic pain, similar changes are seen in the central nervous system. In a phenomenon called ‘wind-up’ (temporal summation), lower stimulation thresholds centrally, along with activation of dormant spinal cord pathways lead to increased nociceptive signals reaching the cortex with escalating intensity. Neural plasticity also develops, resulting in a wider field of receptivity and previously innocuous sensory signals being interpreted as pain. These effects may persist beyond the initial stimuli. Combined, these changes reflect a central sensitization.10
Beyond physiological changes, pain sensitization can have damaging psychological effects. In patients failing to develop adequate coping strategies, depression and disability can ensue.11 As suggested by the biopsychosocial model of pain, it is important to recognize this, as successful management can become more challenging where emotions modulate pain perception.12
Genetics have also been investigated in the pathogenesis of TMD pain. Variations in the gene encoding for the enzyme catecholamine-O-methyltransferase, responsible for the breakdown of catecholamine neurotransmitters, can increase pain sensitivity through activation of b-adrenergic receptors.13 More recently b-adrenergic receptor activation has also been linked with osteo-arthritic processes in the TMJ.14 Finally oestrogen has been implicated, since higher levels are associated with increased muscle and joint pain. The mechanisms are not understood, but oestrogen receptor polymorphisms have been suggested.15
Pharmacological agents
A broad range of medications has been suggested to help manage both acute and chronic TMD. Broadly speaking these can be categorized as:
Analgesics;
Anti-inflammatories;
Muscle relaxants and anxiolytics;
Neuromodulatory agents;
Miscellaneous agents.
It is vitally important to remember that before prescribing any medications, taking a thorough medical history will help prevent drug interactions and adverse reactions, particularly in those with complex medical backgrounds.
Analgesics
Simplistically, analgesics can be further categorized as opioid or non-opioid. The most common non-opioid analgesic available is paracetamol. Alternative routine non-opioid analgesics are included in the other listed categories in accordance with their primary mechanisms of action.
Paracetamol
Paracetamol is a weak inhibitor of the cyclo-oxygenase (COX) enzymes 1 and 2. This reduces prostaglandin production resulting in its weak anti-inflammatory properties (Figure 2). Centrally, it is thought to activate descending serotonergic pathways that are responsible for the majority of its analgesic effect.16 There is limited evidence specific to its use in TMD, but reviews looking at its efficacy in chronic pain have questioned its benefit, showing that in isolation, paracetamol tends to provide inadequate analgesia.17 Nevertheless, it is a readily available drug with proven analgesic effects and therefore can be used short term as a supplementary agent, or where alternatives are contraindicated.1
Figure 2. Arachidonic acid breakdown pathway leading to the formation of the prostaglandins and other various inflammatory mediators. The COX enzyme therapeutic targets are shown.
Opioids
Opioids are endogenous to the body and are produced synthetically for medicine. From an analgesic perspective they activate descending anti-nociceptive pathways to moderate pain signals.18 Common opioids include codeine, tramadol, morphine, oxycodone and fentanyl. Their benefit in chronic pain is well documented, but there is a lack of evidence to recommend or refute their efficacy in the management of TMD.19
The use of opioids for the long-term management of non-oncological chronic pain is controversial.20 This is mainly due to the significant side effects, which include respiratory depression, constipation, urinary retention, sedation and dependency.
Oxycodone has been suggested as the preferred choice for TMD because it is easier to titrate than morphine and has fewer side effects.19 However, oxycodone is a potent pain killer and highly addictive, so should be exclusively reserved for extreme cases where analgesia has been escalated by a suitably trained physician. Tramadol is an alternative opioid analgesic that additionally activates non-opioid analgesic mechanisms. It has a lower affinity for opioid receptors and therefore has a safer risk profile than oxycodone. Prescribers may favour it as a first-line choice as it is lower down the World Health Organization's analgesic ladder, although anecdotally it appears relatively ineffective in the management of chronic TMD pain.19
Fundamentally, if considering this class of medication, specialist medical input from a pain team is necessary, and other interventions and medications should first have been exhausted.
Anti-inflammatories
Non-steroidal anti-inflammatory drugs (NSAIDs)
NSAIDs are commonly used for pain relief and control of inflammation. They inhibit COX enzymes more potently that paracetamol (Figure 2) and can be either selective or non-selective for COX-2.21 NSAIDs have a wide therapeutic window, but prolonged use can lead to significant side effects, such as peptic ulceration and acute kidney injury. COX-2 enzymes are upregulated in inflammatory conditions and so selective inhibition may be more useful. However, the COX-2 enzyme regulates renal mechanisms of water and sodium retention, so inhibition can increase the risk of hypertension and cardiovascular incidents.21
Considering the mode of action, NSAIDs are suitable medications where there is an inflammatory component in the pathogenesis. Commonly prescribed medications, such as ibuprofen, naproxen and diclofenac, have varied efficacy in symptom control in a range of TMD diagnoses, although studies do not show consistently better results over placebos.22,23 Ibuprofen is considered effective in the management of mild–moderate osteoarthritis; however, there is only limited evidence relating to degenerative TMJ disease23,24 or myofascial pain.25 Conversely, one study reported naproxen was effective in pain control for disc displacement.26 Importantly this study highlighted a statistical difference in pain reduction between the intervention and placebo only after 3 weeks, demonstrating time is required for these medications to achieve their full potential. Alternatively, topical formulations of ibuprofen and diclofenac may reduce systemic side effects and potentially have additional anti-nociceptive mechanisms.27 Overall, weak evidence exists to support NSAID use in the management of TMD, although is insufficient to define optimal dosages and durations.23 Nevertheless, it is accepted that they may be useful for short periods of time as part of initial management.1,20
Corticosteroids
Corticosteroids are potent anti-inflammatory agents that suppress the activation of multiple pro-inflammatory genes. They are predominantly used intra-articularly during joint surgery and, as such, will be addressed later in this series.20
Muscle relaxants/anxiolytics
Primarily these drugs are prescribed in acute myofascial pain conditions to control muscle hyperactivity and stop painful muscle spasms. Both classes have muscle relaxant properties, but the sedative effect of anxiolytics may additionally benefit anxiety control and sleep quality, which are linked with pain resilience.28,29 Moreover, they may have some direct analgesic properties.30
Muscle relaxants
Muscle relaxants may be peripherally or centrally acting. Examples include cyclobenzaprine, tolperisone, tinzadine and baclofen. The few controlled clinical trials generally show a limited benefit of these medications compared to no treatment controls,22,30 although a recent network meta-analysis did report a potential benefit from cyclobenzaprine.31 Apropos of the literature, many systemic muscle relaxants carry significant side effects (eg dry mouth, sedation, depression, constipation, etc) and most of the studied agents are either not licensed in the UK for acute muscle spasm management or not available.
Benzodiazepines
Benzodiazepines are a class of anxiolytics that act by enhancing the activity of the neurotransmitter GABA (γ-aminobutyric acid), reducing the excitability of neurones within the central nervous system. Their use in the management of TMD has been investigated more than other medications, but evidence is still limited. Results are conflicting, with both positive25 and negative22,31 outcomes, making it difficult to demonstrate a strong benefit. Although their routine use is arguable, if considering this type of medication, clinicians should remember that they are controlled drugs with the possibility for significant sedation and potential dependency.32 For this reason, only short-term prescriptions in acute presentations of myofascial pain are advocated.1,20
Botulinum toxin (type A)
Botulinum toxin type-A (Bot-A), commonly known under the trade name Botox, is frequently used in facial aesthetic treatment,33 but also has a role in TMD management. Bot-A is a potent inhibitor of presynaptic acetylcholine release, thus preventing muscle contractions. It is also known to reduce nociceptive neuropeptide release.34 The myorelaxant effect is proposed as the main pain relief mechanism, hence Bot-A is typically used to manage myofascial pain.35 The effects of the toxin are temporary with maximal onset occurring around 1 month and synaptic inhibition overcome around 3 months.35 Interestingly, the results of systematic reviews do not show the anticipated positive outcomes, offering only limited benefit, if any, over placebos alone.34 Recently, a larger three-armed randomized study not included in these reviews compared Bot-A against occlusal splints and both in combination. Although the study lacked a true control, the results showed a significant reduction in pain scores for Bot-A and combined treatment group compared to stabilization splints alone over a 6-month period.36
Being most accessible, the temporalis and masseter muscles are the most frequent targets. Injections into the lateral pterygoid muscles have also been advocated for clicks related to disc displacements, recurrent dislocations and myofascial pain, but are technically more challenging.35 Bot-A is generally a safe therapy; however, the risk of lateral spread to adjacent structures or interactions with certain medications are recognized risks.35
Although the overall clinical effectiveness is somewhat spurious, Bot-A is used by many clinicians for refractory cases of local myalgia failing to respond to reversible measures, where results may be more pronounced.37
Neuromodulatory agents
The use of neuromodulatory agents for managing chronic orofacial pain stems from their proven effectiveness in other pain conditions.38 More evidence exists for older therapeutics such as tricyclic antidepressants.38 Extrapolated evidence for anticonvulsants used to manage chronic pain is less convincing, with only an additional 1–2 people in 10 achieving greater than 50% pain reduction over placebos.39 Selective serotonin reuptake inhibitors (SSRIs) and selective serotonin and noradrenaline re-uptake inhibitors (SSNRIs) have also been examined for their pain-relieving effects. Their benefits include a lower side-effect profile, but efficacy appears to be inferior and, paradoxically, they can induce bruxism.30,40 Although neuromodulator efficacy is poorly studied in chronic TMD pain control,41 some positive outcomes are reported for amitriptyline42 and gabapentin.43 Interpretation should be made cautiously as most studies have substantial biases, small sample sizes and/or short follow up. A further challenge is that study populations generally display heterogeneous diagnoses and so, discerning in which circumstances medications are most useful, is difficult.
The mechanism of action of antidepressants is not fully clear. It is thought that their ability to block noradrenaline and serotonin moderates ascending and descending pain pathways, accounting for much of the anti-nociceptive effects.20 Anticonvulsants work in a different manner by decreasing expression of neuronal voltage-gated calcium channels, thus inhibiting impulse transmission.44 The major benefit of anticonvulsants is their improved safety profiles, although both drug classes have side effects.32 It should also be noted that these anticonvulsants have a risk of dependency, and are controlled drugs. Commonly reported difficulties in neuromodulator tolerance are drowsiness, blurred vision, dry mouth, constipation and postural hypotension.20
It can be concluded that neuromodulators are best suited to situations resistant to conservative management, when there is a desire to avoid surgery or it has been unsuccessful, and where there is an element of neuropathic pain, or evidence of central sensitization.
As neuromodulators are also used to manage anxiety and depression, it can be hypothesized they could moderate psychological and social aspects of pain. Patients with concomitant symptoms may therefore be candidates, but this judgement should be made in liaison with their physician.
Miscellaneous agents
Beta-blockers
Following experimental work implicating beta-adrenergic receptor activation in increased pain sensitivity, it was hypothesized that using beta-blockers could reduce pain. A recent clinical study showed promising results, reporting for every six people treated, one patient had a 50% reduction in pain over 9 weeks.45 Additionally, although not anxiolytics per se, beta-blockers are used in the management of anxiety, and so may also affect non-nociceptive components of pain. Currently this medication is still in the experimental phase and not yet accepted in clinical practice.
Immunotherapy
Immunotherapy-based treatments involve the administration of specific antibodies against defined targets. Although gaining popularity in other disciplines, their relevance in TMD is restricted to particular degenerative conditions (eg rheumatoid arthritis), where their use forms a part of wider disease management.21
Conclusion
Pharmacology plays an important but relatively small role in the management of TMD. The major challenge is defining when, and what that role is. The quality of scientific evidence is generally poor, so most recommendations are empirical, based upon expert opinion and theoretical reasoning. It is also difficult to recommend medications as first line treatments over reversable measures where there are known side effects and results are unproven. Another challenge is both the emotional and psychological aspects of pain, combined with the pathophysiological complexity, make any response to medication unique to the individual. As such a ‘one size fits all’ approach is inappropriate and alternatives, or combinations with other measures, may be required. Advances in the understanding of pain, may lead to personalized management approaches and increase the relative importance of pharmacology in the future.
A summary of suggested usages for medications based on current guidance, the presented evidence and the authors practice is presented in Table 1.
Medication type
Suggested use
Usual adult dosage
NSAIDS and analgesics
Short course of ibuprofen for cases with inflammatory pathogenesis (7–10 days) alongside other reversible management options – can combine with paracetamol if needed
400 mg QDS ibuprofen 1000 mg (QDS) paracetamol 5% gel (TDS) ibuprofen 1–3% gel (BDS/TDS) diclofenac
Topical ibuprofen/diclofenac gel may be more useful for acute myofascial pain, but review after initiation as can cause skin irritation
Long-term courses are not advised. If considering for arthritic changes, then liaise with specialist and/or GP and manage as for osteo-arthritis – possibly consider diclofenac or naproxen
Opioids should be avoided and only reserved for cases of ongoing chronic pain where all other treatments have failed. Specialist pain team should ideally be involved
Muscle relaxants and benzodiazepines
Diazepam can be considered for acute episodes of muscular origin with reduction in opening. Doses should be kept low and short (maximum 10 mg for no longer than 2 weeks) to avoid long-term dependency. Preferably to be taken just before bed
5–10 mg (ON) diazepam
Limited evidence for systemic muscle relaxants and most researched medications are not available or advocated in the UK
Botulinum toxin
Not first-line treatment. Reserved for cases of muscular origin failing to respond to conventional treatment. Better response might be seen in localized cases of myalgia. Further training is required and specialist input is advised
25–50 units per site to a maximum of 200 units (unlicensed)
Neuromodulators
Should be reserved for cases unsuccessfully treated with reversible management options and where chronic pain exists with suspected central sensitization or depressive symptoms
Recommended to be prescribed in conjunction with a specialist and through the patient's GP
Amitriptyline tried first. If ineffective or unsuitable, then consider nortryptiline, gabapentin or pregabalin. Dosage increased slowly to titrate to pain control or until side effects are tolerable
BDS: twice daily; OD: once daily; ON: every night; QDS: four times daily; TDS: three times daily.
