Learning objectives.
By reading this article, you should be able to:
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Describe the aetiology and epidemiology of temporomandibular disorders (TMD).
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Undertake a simple assessment and examination to allow diagnosis of TMD.
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Discuss the basic management techniques for TMD and when referral to specialists is indicated.
Key points.
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Temporomandibular disorders (TMD) is the collective term for a group of musculoskeletal conditions involving pain, dysfunction, or both in the masticatory muscles, temporomandibular joints (TMJ), and their associated structures.
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The pathophysiology of common painful TMD is biopsychosocial and multifactorial.
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Early diagnosis and management of TMD is likely to greatly improve prognosis and quality of life, and reduce healthcare and wider economic costs.
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Certain sinister or significant diagnoses may present with similar symptoms to TMD; clinicians should be aware of these ‘red flags’.
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Conservative techniques are effective in the management of TMD. When indicated, some patients may benefit from specialist referral and multidisciplinary management.
Introduction
Temporomandibular disorders (TMD) have been known by a variety of different names over the years including facial arthralgia, pain dysfunction syndrome, ‘TMJD’, ‘TMJ’ and Costen's syndrome.1 The currently accepted term is temporomandibular disorders. It is important to note TMD is not a diagnosis; it is the collective term for a group of differing musculoskeletal conditions involving pain, dysfunction, or both in the masticatory muscles, temporomandibular joints (TMJ) and associated structures.2
Temporomandibular disorders are the most common type of non-odontogenic orofacial pain and have the potential to produce persistent (chronic) pain.3 Individuals with TMD commonly also have other painful and non-painful comorbidities including headaches, fibromyalgia, irritable bowel syndrome, tinnitus, chronic fatigue syndrome, depression and sleep disturbance.4 As seen with other chronic pain conditions, TMD are influenced by biopsychosocial factors.5
Early diagnosis and management of TMD can greatly improve prognosis and quality of life for patients.3 Efficient care pathways and the establishment of multidisciplinary treatment centres are required to ensure that treatment-seeking patients are recognised and treated accordingly, reducing overall healthcare costs.6
Epidemiology
It has been estimated that 4% of TMD-free adults aged 18–44 yrs develop clinically confirmed primary onset painful TMD each year. The incidence of TMD increases with age, peak incidence being reported as 4.5% within the 35–44 yr old age group.5 Females are only slightly more likely to be affected than males, but are more likely to develop persistent TMD.7 Significant differences have been reported in the pattern of prevalence, depending on age, between ethnic groups. Non-Hispanic white females have increased prevalence in younger age, with prevalence decreasing after the age of 50 yrs; conversely non-Hispanic black women have a lower prevalence at younger ages but the prevalence increases up to 55–64 yrs of age.8 Interestingly, there appears to be little association between socioeconomic group and TMD incidence as is seen with other chronic painful conditions.3,7
A large prospective cohort study comprising children aged 11–14 yrs estimated a yearly incidence of 2.3% for clinically confirmed diagnosis of TMD. This study also identified a number of risk factors associated with predicting the onset of TMD including female sex, presence of somatic symptoms, number of existing pain conditions and life dissatisfaction. No correlation was made between race and clinically confirmed TMD; however, those adolescents who reported their race as white were significantly more likely to experience an onset of facial pain not meeting diagnostic criteria for TMD than those who reported their race as black or ‘other’.9
Aetiology and pathophysiology
The cause and underlying pathophysiology of TMD has been a matter of much debate over the years. It is now understood that TMD is a complex disorder with multiple causes and, as with other forms of chronic pain, TMD is consistent with a biopsychosocial model of illness.5 An individual's psychological profile and their sensitivity to pain has been found to influence their susceptibility to TMD.10 Further to this, global symptoms such as other comorbid conditions (e.g. irritable bowel syndrome, insomnia, headache and fibromyalgia) and orofacial symptoms are strong predictors for the development of TMD.4 Furthermore, certain clinical measures that can be assessed at presentation have been found to play a contributing part in increasing the likelihood of developing persistent TMD such as masticatory muscle and TMJ pain that is familiar on mandible mobility.11
Putative mechanisms
Although it is known that biological, psychological and social factors combine to predispose, initiate or perpetuate painful TMD, the exact pathophysiology remains unclear. Several mechanisms have been suggested that may interact with one another to contribute to painful TMD. The mechanisms suggested below can also explain the presence of painful and non-painful comorbidities in patients with TMD.
A study examining single-nucleotide polymorphisms (SNP) revealed associations between genetic risk factors for clinical, psychological and sensory phenotypes and the onset of TMD. A total of 3295 SNP representing 358 genes linked to pain perception were examined and five SNP were found to be significantly predictive of TMD and pain incidence.12
Catecholamine-O-methyltransferase (COMT) activity has been found to substantially influence pain sensitivity and TMD onset via adrenergic pathways. This enzyme has broad biological functions including regulation of catecholamines and enkephalins, which are involved with many neurological functions. Females with particular genetic variants (haplotypes) causing decreased activity of COMT were found to have significantly increased pain sensitivity and be 2.3 times more likely to develop TMD.13
Pro- and anti-inflammatory cytokines have also been found to contribute to the pathophysiology of TMD in genetically susceptible individuals. Specifically, increased circulating concentrations of pro-inflammatory monocyte chemotactic protein (MCP-1), reduced transcription of anti-inflammatory transforming growth factor-1 (TGF-1) were found in patients with painful TMD.14 In addition, calcitonin gene-related peptide (CGRP), a neuropeptide released from trigeminal nerves, mediates neurogenic inflammation. Increased CGRP concentrations within the joint capsule, seen in patients with TMD, is thought to cause inflammation and pain by stimulation of peripheral and central sensitisation.15
These specific pathways and mechanisms that may predispose, initiate or perpetuate persistent painful TMD within an individual do not work independently. They are likely to interplay, leading to increased excitability and synaptic efficacy of neurones in peripheral and central nociceptive pathways. This process is known as peripheral and central sensitisation, and for TMD this has been shown to manifest as sensitisation of trigeminal neurones and enhanced pain signalling.16 Patients with increased peripheral and central sensitisation are also more likely to suffer from other types of persistent pain including headache and fibromyalgia; hence these conditions often coexist in patients with TMD.4
Clinical features and diagnosis
Presentation
Patients with TMD can present with any or all of the following signs and symptoms: pain in the TMJ or muscles of mastication that may radiate or refer to local or distant structures; clicking, locking or crepitus of the TMJ on any of its movements with or without locking of the joint; headache within the temporal region; and otalgia or tinnitus or both in the absence of aural disease.3 Symptoms tend to be recurrent in the majority of patients (65%) and related to the orofacial region (71.1%) although a sizeable proportion (23%) only present with headache.7
Diagnosis
Over the past decades there have been different forms of assessments proposed for TMD. The most widely recognised of these diagnostic tools is the Diagnostic Criteria for Temporomandibular Disorders (DC/TMD).17 The DC/TMD aims to provide a standardised and operationalised tool which encompasses physical examination of the masticatory structures (axis I) and screening for psychosocial and comorbid factors (axis II) to allow diagnosis of TMD.
Screening
A screening questionnaire, known as the TMD Pain Screener has been developed to be used in tandem with the DC/TMD or in isolation in non-specialist settings. It is suggested that the screening tool be used by medical professionals to aid and inform their decision to refer patients to an appropriate service. The questionnaire (Fig 1) is also freely available on the International Network for Orofacial Pain and Related Disorders Methodology website (https://ubwp.buffalo.edu/rdc-tmdinternational/wp-content/uploads/sites/58/2017/01/TMD-Pain-Screener_revised-10Aug2011.pdf).
Figure 1.
TMD pain screener. A score of ≥3 indicates a positive finding and must be followed by a more comprehensive evaluation to establish diagnosis.
Axis I
Axis I of the DC/TMD encompasses a specific standardised physical examination to allow diagnosis. There are 38 defined types of TMD diagnoses, of which 12 are most common. Table 1 displays these 12 most common types of diagnosis which have established sensitivity and specificity.17 To simplify the diagnoses further and aid in recall, the 12 diagnosis displayed in Table 1 can be divided into four groups of myalgia, arthralgia, intra-articular disorders and headache attributable to TMD. These diagnoses are not mutually exclusive, and an individual can present with multiple simultaneous painful TMD diagnosis, non-painful TMD diagnosis, or both. Full details of the DC/TMD algorithms and decision trees are available on the International Network for Orofacial Pain and Related Disorders Methodology website.
Table 1.
Summary of salient history and examination findings for 12 most common temporomandibular disorders.17
| Category | Subcategory | Summary history and examination findings |
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Pain local to palpation; pain within body of muscle; pain spreading outside the body of muscle |
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Pain in temporomandibular joint region produced by one of: palpation or assisted or unassisted jaw movements | |
| Inter-articular disorders | Disc displacements:
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Click, pop, snap: on open and close (1 out of 3 movements), or one of opening and closing plus a lateral movement; as above but history of lock does not matter how long; history: decreased mouth opening and inability to eat or interference with eating. Examination: maximum assisted opening <40 mm; history as above but maximum assisted opening >40 mm |
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Crepitus in any movement, with relatively little pain | |
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History: lock open and self-manipulation to achieve closure | |
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History: headache in temple and modified with jaw movement, function or parafunction. Examination: familiar headache with palpation temporalis or with jaw movements |
The revised and validated DC/TMD criteria are based upon the concept of eliciting pain that is ‘familiar’. Familiar pain is the process of recreating the patient's symptoms during an examination and confirming with them that this is what they experience.17 Further to this, the DC/TMD contains an algorithm to indicate when diagnostic imaging is required. Most of the diagnoses can be confirmed based upon clinical examination and history alone, and further imaging is generally considered when a functional problem is indicated. Imaging generally comprises MRI for intra-articular disorders or CT for degenerative joint disorder.17
Axis II
It is known that patients with TMD present with a higher psychosocial burden and frequency of comorbid conditions.4,10 The presence of factors such as depression, and catastrophising can influence severity of pain, prognosis and treatment outcome.18 Axis II of the DC/TMD contains recommended instruments for screening and for a comprehensive assessment. These instruments aim to assess pain behaviours, psychological status and level of function allowing contributory factors to be highlighted and treatment to be tailored accordingly.17 It is suggested that the simpler screening tools are used by medical professionals to identify those that require more comprehensive assessment or onward referral.
A further axis of diagnosis (axis III) has been suggested to represent the underlying pathobiologic processes contributing to the TMD phenotype, currently absent from DC/TMD. This axis would incorporate diagnostic findings from genetics, epigenetics and neuroscience to improve in disease diagnosis and improve targeted management.19
‘Red flags'
TMD generally follow a benign and non-progressive course; however, it is very important that the clinician is aware of certain significant or sinister diagnoses which may present similarly to TMD.20 Fig 2 outlines ‘red flags’ that may mimic TMD and if present should be used to aid differential diagnosis and possible referral to the appropriate specialist. Referral to oral medicine, oral (and maxillofacial) surgery, ENT, neurology or neurosurgery may be considered depending on the anatomical region or symptoms.
Figure 2.
‘Red flag’ signs or symptoms presenting as TMD that may indicate a separate, significant or sinister diagnosis.
Management
International consensus recommends that reversible conservative therapies are used as the first line of treatment for TMD.21 This recommendation is founded on data which demonstrate that between 75% and 90% of patients will respond to less invasive management techniques.22 As TMD are of complex multifactorial aetiology, often a strategy of treatment including biological, psychological and social aspects of care is required.3,21 Furthermore, it is known that the presence of psychosocial factors can predict a poorer long-term prognosis and greater likelihood of the development of persistent pain; therefore, the recognition and prompt treatment of psychosocial distress is advisable.18
Reversible or conservative treatment
Education
A patient's uncertainty around the diagnosis of TMD can significantly affect their quality of life and may lead to care pathways that are unsuccessful, or aggravate the presenting complaint further.23 It is therefore very important to educate patients on the usually non-progressive and benign nature of TMD at an early stage. A full description of the (provisional) diagnosis should be given to the patient including an explanation of the complex aetiology and impact of psychosocial factors. Fig. 3 displays a list of available resources, suggested by the National Institute for Health and Care Excellence (NICE), that can be used by medical professionals to aid patient education.21
Figure 3.
List of resources for clinicians to aid in the education of patients with TMD.
Self-care techniques
Guidance published in accordance with the Royal College of Surgeons for primary care details specific suggestions for self-management of TMD.3 Soft diet and jaw rest during an acute exacerbation is advised. Discontinuation of parafunctional habits (nail biting, teeth grinding or clenching, gum chewing), reduced caffeine consumption and improved sleep hygiene are advised to prevent exacerbation of the condition. Symptomatic relief of musculature via direct application of cold or warm packs may also be beneficial. Lastly, diaphragmatic breathing exercises and meditation can aid in overall relaxation and build resilience.3
Intraoral appliances
A splint (either soft polyethylene or hard acrylic) worn over the upper or lower teeth is a widely recognised treatment for TMD. A recent network meta-analysis found that the wearing of a stabilisation appliance has a significant treatment effect beyond placebo. Participants in the stabilisation splint category reported significant improvement in treatment satisfaction and reduced pain intensity when compared with those treated with non-occluding appliances (active placebo) or untreated participants.24
Physical therapy and acupuncture
There is limited evidence to suggest the benefits of physiotherapy including targeted exercises or massage for management of TMD. However, a proposed Cochrane review into this topic is awaited.25 A recent network meta-analysis has found that acupuncture provides no treatment effect for myofascial pain of the masticatory muscles in TMD when compared with dry needling or wet needling using different substances.26 However, once again, the quality of evidence within these reviews is low, and there is a need for further robust clinical trials.
Psychological management
Although all TMD conservative treatment strategies incorporate an element of psychological management, some patients may benefit from specialist input from a clinical psychologist. Patients with major psychological symptoms, predominantly anxiety and depression, have been found to obtain more improvement of TMD pain with multidisciplinary treatment compared with patients without psychological symptoms.27 A psychologist may use a range of interventions to aid with pain management including cognitive behavioural therapy (CBT) and biofeedback. A recent systematic review and meta-analysis found that CBT was effective for improvement in long-term pain intensity, depression, muscle palpation tenderness and reduced interference with daily activity when compared with ‘usual care’ (education, counselling and splint therapy).28 Biofeedback and relaxation training were found to yield similarly improved results compared with active controls.27 Where indicated, patients should be referred to a psychologist as soon as possible to allow for prompt management.3
Pharmacotherapy
A range of pharmacological treatments are recognised for TMD including simple analgesics, neuromodulatory agents and intramuscular injectables. As for other chronic pain conditions, drug therapy should be used in conjunction with other interventions, and all potential risks, adverse effects and interactions of the drug should be considered before prescription.3
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Simple analgesics: NSAIDs have been shown to be an effective treatment for chronic TMD joint pain after a systematic review and network meta-analysis.29 The same review also supported the short-term use of the centrally acting skeletal muscle relaxant cyclobenzaprine for TMD muscle pain, and two included studies considered the possible effects of Ping-On ointment and melatonin.29
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Neuromodulatory agents: tricyclic antidepressants, serotonin–noradrenaline reuptake inhibitors and gabapentin, can be used off-licence for treatment of complex TMD cases.30 The evidence to support the pharmacotherapeutic response of these medications for TMD is limited with extrapolations often made from studies examining their effectiveness in other chronic pain conditions.21 Further to this, common comorbid conditions to TMD including headache, sleep disturbance and anxiety should be considered before prescription.30
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Botulinum toxin (BoNT): it is hypothesised that BoNT reduces muscle contracture, inhibits the release of inflammatory mediators and has a direct effect on nociceptors, reducing central pain sensitisation. However, a recent network meta-analysis has found no clear evidence for intramuscular BoNT injection for TMD muscle pain compared with acupuncture or dry needeling.26
Irreversible and invasive treatment
Surgical management
Interventions including arthroscopy, arthrocentesis, arthroplasty or joint replacement can be considered for patients with arthrogeneous TMD.21 There is insufficient robust evidence to support their use to treat the 12 most common types of TMD, and invasive procedures such as arthroplasty or complete joint replacement can be associated with significant morbidity.27 Therefore, to allow appropriate justification, these invasive surgical procedures should be restricted to cases where all other conservative techniques have failed.27
Secondary care or specialist management
Referral to secondary care is suggested if the diagnosis of TMD is unclear or if symptoms have persisted or worsened over 3 months despite primary reversible treatment. Further to this, if there is marked psychological distress associated with symptoms or if there is unexplained persistent pain or chronic widespread pain, secondary care referral should be considered as these factors are associated with a poor long-term prognosis.18,21
Research suggests that patients may benefit from the establishment of specialist regional centres for chronic orofacial pain. These centres would allow a biopsychosocial framework of care to be delivered to severe cases of TMD with input from several specialties, including anaesthetists.6
Conclusion
TMD are a complex set of disorders that can often lead to chronic pain. As advances within research are made, a greater understanding of the multifactorial aetiology of painful TMD is developing. This will likely lead to the development of improved TMD prevention, diagnosis and treatment strategies which are aimed at individual mechanisms and contributing factors. A biopsychosocial framework of care is advised to treat TMD encompassing a multidisciplinary approach through a single integrated treatment pathway. Research suggests that the establishment of specialist regional centres for orofacial pain might provide a more streamlined and cost-effective management approach within secondary or tertiary care.
Declaration of interests
The authors declare that they have no conflicts of interest.
MCQs
The associated MCQs (to support CME/CPD activity) are accessible at www.bjaed.org/cme/home by subscribers to BJA Education.
Biographies
Julia Palmer MJDF RCS(Eng) PG Cert Dent(Ed) is an academic clinical fellow in oral surgery at Newcastle upon Tyne Dental Hospital and Newcastle University. She is a member of the International Association of Dental Research and INfORM.
Justin Durham MFDS RCD(Ed) PhD FDS (OD) RCS is head of the School of Dental Sciences and professor of orofacial pain and honorary consultant oral surgeon at Newcastle upon Tyne Dental Hospital. Professor Durham is president-elect of INfORM and an elected member of the European Academy of Craniomandibular Disorders. His current research programmes include acute inflammatory dental pain and persistent orofacial pain.
Matrix codes: 1A01, 2E03, 3A02
Footnotes
Supplementary data to this article can be found online at https://doi.org/10.1016/j.bjae.2020.11.001.
Appendix A. Supplementary data
The following is/are the supplementary data to this article:
References
- 1.Costen J.B. A syndrome of ear and sinus symptoms dependent upon disturbed function of the temporomandibular joint. Ann Otol Rhinol Laryngol. 1997;106:805–819. doi: 10.1177/000348949710601002. [DOI] [PubMed] [Google Scholar]
- 2.List T., Jensen R.H. Temporomandibular disorders: old ideas and new concepts. Cephalalgia. 2017;27:692–704. doi: 10.1177/0333102416686302. [DOI] [PubMed] [Google Scholar]
- 3.Durham J., Aggarwal V., Davies S. Temporomandibular disorders(TMDs): an update and management guidance for primary care from the UK Specialist Interest Group in Orofacial Pain and TMDs (USOT) R Coll Surg Fac Dent Surg. 2013:1–22. https://www.rcseng.ac.uk/dental-faculties/fds/publications-guidelines/clinical-guidelines/ Available from: [Google Scholar]
- 4.Hoffmann R.G., Kotchen J.M., Kotchen T.A., Cowley T., Dasgupta M., Cowley A.W. Temporomandibular disorders and associated clinical comorbidities. Clin J Pain. 2011;27:268–274. doi: 10.1097/AJP.0b013e31820215f5. [DOI] [PubMed] [Google Scholar]
- 5.Slade G.D., Fillingim R.B., Sanders A.E. Summary of findings from the OPPERA prospective cohort study of incidence of first-onset temporomandibular disorder: implications and future directions. J Pain. 2013;14:T116–T124. doi: 10.1016/j.jpain.2013.09.010. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Breckons M., Bissett S.M., Exley C., Araujo-Soares V., Durham J. Care pathways in persistent orofacial pain. JDR Clin Transl Res. 2017;2:48–57. doi: 10.1177/2380084416679648. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Slade G.D., Bair E., Greenspan J.D. Signs and symptoms of first-onset TMD and sociodemographic predictors of its development: the OPPERA prospective cohort study. J Pain. 2013;14:T20–T32. doi: 10.1016/j.jpain.2013.07.014. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Isong U., Gansky S.A., Plesh O. Temporomandibular joint and muscle disorder-type pain in U.S. adults: the National Health Interview Survey. J Orofac Pain. 2008;22:317–322. [PMC free article] [PubMed] [Google Scholar]
- 9.LeResche L., Mancl L.A., Drangsholt M.T., Huang G., Korff M Von. Predictors of onset of facial pain and temporomandibular disorders in early adolescence. Pain. 2007;129:269–278. doi: 10.1016/j.pain.2006.10.012. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.Maixner W., Diatchenko L., Dubner R. Orofacial pain prospective evaluation and risk assessment study — the OPPERA study. J Pain. 2011;12:T4. doi: 10.1016/j.jpain.2011.08.002. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Meloto C.B., Slade G.D., Lichtenwalter R.N. Clinical predictors of persistent temporomandibular disorder in people with first-onset temporomandibular disorder: a prospective case-control study. J Am Dent Assoc. 2019;150:572–581. doi: 10.1016/j.adaj.2019.03.023. e10. [DOI] [PubMed] [Google Scholar]
- 12.Smith S.B., Mir E., Bair E. Genetic variants associated with development of TMD and its intermediate phenotypes: the genetic architecture of TMD in the OPPERA prospective cohort study. J Pain. 2013;14:T91. doi: 10.1016/j.jpain.2013.09.004. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13.Diatchenko L., Slade G.D., Nackley A.G. Genetic basis for individual variations in pain perception and the development of a chronic pain condition. Hum Mol Genet. 2005;14:135–143. doi: 10.1093/hmg/ddi013. [DOI] [PubMed] [Google Scholar]
- 14.Slade G.D., Conrad M.S., Diatchenko L. Cytokine biomarkers and chronic pain: association of genes, transcription, and circulating proteins with temporomandibular disorders and widespread palpation tenderness. Pain. 2011;152:2802–2812. doi: 10.1016/j.pain.2011.09.005. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Cady R.J., Glenn J.R., Smith K.M., Durham P.L. Calcitonin gene-related peptide promotes cellular changes in trigeminal neurons and glia implicated in peripheral and central sensitization. Mol Pain. 2011;7:94. doi: 10.1186/1744-8069-7-94. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.La Touche R., Paris-Alemany A., Hidalgo-Pérez A., López-de-Uralde-Villanueva I., Angulo-Diaz-Parreño S., Muñoz-García D. Evidence for central sensitization in patients with temporomandibular disorders: a systematic review and meta-analysis of observational studies. Pain Pract. 2018;18:388–409. doi: 10.1111/papr.12604. [DOI] [PubMed] [Google Scholar]
- 17.Schiffman E., Ohrbach R., Truelove E. Diagnostic criteria for temporomandibular disorders (DC/TMD) for clinical and research applications: recommendations of the international RDC/TMD consortium network and orofacial pain special interest group. J Oral Facial Pain Headache. 2014;28:6–27. doi: 10.11607/jop.1151. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 18.Velly A.M., Look J.O., Carlson C. The effect of catastrophizing and depression on chronic pain — a prospective cohort study of temporomandibular muscle and joint pain disorders. Pain. 2011;152:2377–2383. doi: 10.1016/j.pain.2011.07.004. [DOI] [PubMed] [Google Scholar]
- 19.Ohrbach R., Dworkin S.F. The evolution of TMD diagnosis: past, present, future. J Dent Res. 2016;95:1093–1101. doi: 10.1177/0022034516653922. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20.Beddis H.P., Davies S.J., Budenberg A., Horner K., Pemberton M.N. Temporomandibular disorders, trismus and malignancy: development of a checklist to improve patient safety. Br Dent J. 2014;217:351–355. doi: 10.1038/sj.bdj.2014.862. [DOI] [PubMed] [Google Scholar]
- 21.Temporomandibular disorders (TMDs) — NICE CKS. 2020. https://cks.nice.org.uk/temporomandibular-disorders-tmds#!scenario Available from: [Accessed date: 18 June 2020] [Google Scholar]
- 22.Greene C.S. The etiology of temporomandibular disorders: implications for treatment. J Orofac Pain. 2001;15:117–145. [PubMed] [Google Scholar]
- 23.Durham J., Steele J., Moufti M.A., Wassell R., Robinson P., Exley C. Temporomandibular disorder patients’ journey through care. Community Dent Oral Epidemiol. 2011;39:532–541. doi: 10.1111/j.1600-0528.2011.00608.x. [DOI] [PubMed] [Google Scholar]
- 24.Alkhutari A.S., Alyahya A., Rodrigues Conti P.C., Christidis N., Al-Moraissi E.A. Is the therapeutic effect of occlusal stabilization appliances more than just placebo effect in the management of painful temporomandibular disorders? A network meta-analysis of randomized clinical trials. J Prosthet Dent. 2020 doi: 10.1016/j.prosdent.2020.08.015. https://gdt.gradepro.org/app/ Available from: [DOI] [PubMed] [Google Scholar]
- 25.Craane B., De Laat A., Dijkstra P.U., Stappaerts K., Stegenga B. Physical therapy for the management of patients with temporomandibular disorders and related pain. Cochrane Database Syst Rev. 2006;2018:CD005621. [Google Scholar]
- 26.Al-Moraissi E.A., Alradom J., Aladashi O., Goddard G., Christidis N. Needling therapies in the management of myofascial pain of the masticatory muscles: a network meta-analysis of randomised clinical trials. J Oral Rehabil. 2020;47:910–922. doi: 10.1111/joor.12960. [DOI] [PubMed] [Google Scholar]
- 27.List T., Axelsson S. Management of TMD: evidence from systematic reviews and meta-analyses. J Oral Rehabil. 2010;37:430–451. doi: 10.1111/j.1365-2842.2010.02089.x. [DOI] [PubMed] [Google Scholar]
- 28.Aggarwal V.R., Fu Y., Main C.J., Wu J. The effectiveness of self-management interventions in adults with chronic orofacial pain: a systematic review, meta-analysis and meta-regression. Eur J Pain. 2019;23:849–865. doi: 10.1002/ejp.1358. [DOI] [PubMed] [Google Scholar]
- 29.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. doi: 10.1111/joor.12539. [DOI] [PubMed] [Google Scholar]
- 30.Haviv Y., Rettman A., Aframian D., Sharav Y., Benoliel R. Myofascial pain: an open study on the pharmacotherapeutic response to stepped treatment with tricyclic antidepressants and gabapentin. J Oral Facial Pain Headache. 2015;29:144–151. doi: 10.11607/ofph.1408. [DOI] [PubMed] [Google Scholar]
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