Clinical synthesis based on the most recent meta-analyses and international consensus statements: DC/TMD, ICOP 2020, OPPERA, the 2023 BMJ practice guideline, 2025 prospective data.

Temporomandibular joint syndrome, more commonly called temporomandibular disorders (TMD) in the modern scientific literature, represents a heterogeneous group of conditions affecting the muscles of mastication, the temporomandibular joint (TMJ) itself and associated structures.¹ This umbrella term covers pain and dysfunction that can have a significant impact on quality of life, including difficulty chewing, speaking or opening the mouth. 😟

How is this condition defined, who does it affect and what are the risk factors?

TMD are defined as musculoskeletal disorders of multifactorial origin.² They present mainly through three cardinal signs: pain in the pre-auricular region (in front of the ear) or in the masticatory muscles, joint sounds (clicking, cracking) during jaw movements, and a limitation or deviation of the range of mandibular movement.³

The prevalence of TMD in the general population is considerable. The most recent estimates (Valesan 2021 meta-analysis, 21 pooled studies) report a prevalence of about 31% in adults and 11% in children/adolescents, with disc displacement with reduction being the most frequent subcategory.⁴ Only a fraction of symptomatic people (about 5 to 7%), however, need active treatment.

Women are disproportionately affected : the Bueno 2018 meta-analysis finds pooled odds ratios of 2.2 for overall TMD, 2.1 for muscle disorders (group I), 1.6 for disc displacement (group II) and 2.1 for arthralgia/osteoarthritis (group III).⁵ The 2025 prospective data from a large Swedish cohort (Lövgren et al., n = 94,769 over 8 years) confirm that women have both a higher rate of transition from “no TMD” to “any TMD symptom” and poorer recovery than men.¹⁵ The peak of incidence lies between 20 and 40 years of age, which makes it a condition mainly affecting young adults and middle-aged adults.⁶

The risk factors associated with the development and persistence of TMD are multiple and interact in complex ways. A recent meta-analysis identified several predominant factors 🧐:

• Psychosocial factors: Stress, anxiety, depression and somatisation are among the most powerful predictors of the onset of TMD and of its progression to chronicity.⁷ These factors can increase muscle tension and lower pain perception thresholds.
• Oral parafunctions: Awake or sleep bruxism (grinding or clenching of the teeth) is associated with muscle pain (myalgia) because of the mechanical overload it places on the masticatory system. An important nuance from the Manfredini & Lobbezoo systematic review: the association is markedly stronger in studies based on self-report / questionnaires than in instrumental studies (electromyography or polysomnography), where the link is weak or even negative. The method used to assess bruxism therefore conditions the clinical interpretation.⁸
• Genetic and hormonal factors: Genetic predispositions influencing pain perception and the inflammatory response are suspected.⁹ The higher prevalence in women also suggests an influence of sex hormones, notably oestrogens.⁵
• Trauma: Macrotrauma (a direct blow to the jaw, whiplash) and repeated microtrauma (chewing on one side only, postural habits) can initiate or aggravate TMD. The 2025 meta-analysis by Häggman-Henrikson finds a mean prevalence of painful TMD of 18.9% in the acute phase and 26.8% in the chronic phase after whiplash, versus 5.7% in controls; prevalence is already high in the acute phase and does not fall towards the chronic phase, which argues for systematic early screening.¹⁰
• Comorbidities: TMD frequently coexist with other chronic pain syndromes such as fibromyalgia, irritable bowel syndrome, tension-type headache and neck pain, suggesting shared sensitisation mechanisms. The 2023 meta-analysis by Yakkaphan reports a prevalence of TMD reaching 76.8 % in fibromyalgia patients, and about 32.7 % for fibromyalgia in TMD patients, especially for myogenous forms.¹¹

What happens in the body and how does temporomandibular joint (TMJ) syndrome evolve naturally?

The pathophysiology of TMD is complex and varies according to whether the disorder is mainly muscular (myogenous) or articular (arthrogenous). In myogenous TMD, a mechanical overload due to bruxism or other parafunctions leads to muscle fatigue, local ischaemia and an accumulation of inflammatory mediators, causing pain and contractures.¹²

In arthrogenous TMD, the process may involve displacement of the articular disc, inflammation of the synovial membrane (synovitis) or degenerative osteoarthritic changes (arthralgia and osteoarthritis).¹³ Intra-articular inflammation (synovitis and capsulitis) is a key feature, leading to the release of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α in particular) that degrade cartilage and sensitise local nerve endings.² A crucial aspect in the transition to chronicity is the phenomenon of central sensitisation. 🧠 Persistent painful stimulation at the TMJ can lead to hyperexcitability of neurons in the central nervous system, which amplifies pain perception and can make it persist even in the absence of a peripheral stimulus. The exploratory MRI study by Younger et al. documented, in patients with chronic myofascial TMD, objectively demonstrable neuroanatomical abnormalities : altered grey matter density in the trigeminal sensory nuclei (pons) and in limbic areas (rostral anterior cingulate, hippocampus), correlated with the severity and duration of pain. ⚠️ A caveat, however: the study involves a small sample (n = 15 female patients vs 15 controls) and is exploratory in nature; the results need confirmation on a larger scale. This neuroanatomical signature nevertheless remains consistent with a pathophysiological model going beyond the articular periphery alone.¹⁴

Regarding the natural course, modern research has made it possible to temper the idea that TMD are an inevitably progressive condition. The natural course is in fact fluctuating, with alternating periods of remission and exacerbation. Two landmark longitudinal studies support this dynamic profile:

• The historic study by Magnusson, Egermark & Carlsson (Sweden, n = 320 subjects followed from the age of 15 to 35) shows that the signs and symptoms of TMD fluctuate over successive assessments, with no systematic tendency towards worsening or towards complete resolution with age; they remain variable from one individual to another and from one decade to another.¹⁶
• The more recent prospective data Lövgren 2025 (Swedish cohort, 8 years, n = 94,769) confirm the dynamic but uneven character: transitions to remission exist, but are less frequent in women, who show both a higher incidence and slower recovery.¹⁵

Only a minority of patients progress to a severe chronic form requiring more specialised interventions. This course, favourable overall but uneven depending on the profile, underlines the importance of an initial therapeutic approach that is conservative, reversible and stratified according to prognostic factors (sex, comorbidities, psychosocial status).

The diagnosis of temporomandibular disorders (TMD), a more precise term than temporomandibular joint syndrome, rests on a systematic and multidimensional approach. To ensure diagnostic certainty and guide treatment effectively, the use of validated diagnostic criteria is essential. The current international reference standard is the Diagnostic Criteria for Temporomandibular Disorders (DC/TMD), which proposes an assessment on two axes for a complete understanding of the patient.¹ Since 2020, this framework has been complemented by the International Classification of Orofacial Pain (ICOP), which integrates TMD into a broadened nosology of nearly 200 orofacial pains, modelled on the structure of the ICHD-3 and now considered the gold standard for research in orofacial pain.⁷

The full DC/TMD remains the reference. An international consensus (Durham 2024) built an abbreviated version, the bDC/TMD (4 sections, 3 movements, 3 sets of palpation, Axis II in 11 items), for non-specialised practices, notably dental ones, and so that it can be tested in the field.¹⁹ Tested retrospectively against the full DC/TMD, on data from examinations already collected, a simplified version identifies painful TMD well (sensitivity 0.88, specificity 0.98), but identifies acute locking, other disc-related TMD and osteoarthritis poorly (sensitivity of 0.12 at most)²⁰; headache attributed to TMD is its weak point.²¹ It has not been evaluated in physiotherapy.

Which questions should you ask to understand the patient and their history?

The patient history is the cornerstone of TMD diagnosis. 🧐 It aims not only to characterise pain and physical symptoms (Axis I), but also to assess the psychosocial impact of the condition (Axis II), a major prognostic and therapeutic factor.¹

The first step often consists of rapid screening. The three-question questionnaire (3Q/TMD), validated in a Swedish population of more than 7,800 individuals, has shown satisfactory diagnostic performance in the general population (sensitivity ≈ 0.86 and specificity ≈ 0.98 for the pain questions; sensitivity 0.48 and specificity 0.96 for the functional question in a specialist clinic).² The 3Q/TMD is now recommended as a triage tool in routine dental and physiotherapy practice.² These questions are:

• Have you had pain in the temple, face, temporomandibular joint or jaw once a week or more in the last 30 days?²
• Have you felt pain or stiffness in your jaw on waking once a week or more in the last 30 days?²
• Have the following activities changed (improved or worsened) your facial or jaw pain once a week or more in the last 30 days: chewing, talking, singing, yawning, moving your jaw?²

If the patient answers positively, a more thorough investigation is needed. The interview should systematically explore:

• Pain characteristics : location, intensity (numerical scale), quality (burning, throbbing, dull ache), frequency and duration.³
• Joint sounds : presence of snapping, clicking or crepitus, and whether these sounds are associated with pain.⁴
• Jaw function : limited mouth opening, locking on opening or closing, and difficulty chewing.⁴
• History of the symptoms : date of onset, triggering factors (trauma, stress, dental treatment), and course over time.
• Oral parafunctions : awareness of tooth clenching (daytime bruxism) or grinding (night-time bruxism), often reported by the partner.⁵
• Axis II assessment : it is crucial to assess psychological distress, anxiety, depression and pain catastrophising using validated scales such as the Graded Chronic Pain Scale (GCPS) or the Patient Health Questionnaire (PHQ).¹,⁶ These factors strongly influence the development of chronicity and the response to treatment.

Which clinical tests should you perform and which other conditions must be ruled out?

The clinical examination, rigorously standardised by the DC/TMD protocol, makes it possible to confirm the hypotheses from the history and to establish a precise Axis I diagnosis.⁴

The essential tests include:

• Measuring range of motion : unassisted maximum mouth opening, lateral movements and protrusion are measured in millimetres. An opening of less than 40 mm is generally considered limited.⁴,⁷
• Palpation of muscles and joints : the DC/TMD protocol specifies a standardised palpation pressure (about 1 kg for the masticatory muscles and 0.5 kg for the TMJ) to identify pain sites.⁷ Palpation of the masseter and temporalis muscles is particularly relevant for the diagnosis of myalgia.⁸ A meta-analysis has shown that the DC/TMD criteria for myofascial pain with referral have a high specificity (0.98), meaning that a positive test almost certainly confirms the condition, although sensitivity is more variable.⁹
• Detection of joint sounds : the examiner listens for sounds (clicks, crepitus) during opening, closing and protrusive movements to diagnose disc displacements.⁴ The reliability of the clinical examination for diagnosing disc displacement with reduction is judged to be moderate to substantial.¹⁰

🎯 The differential diagnosis is a critical step so as not to wrongly attribute symptoms to TMD. The following must be systematically ruled out:

• Dental conditions : abscess, pulpitis, or periodontal disease.
• Primary headaches : migraine, tension-type headache. It is important to note that TMD can themselves cause "headaches attributed to TMD".⁷
• Facial neuralgias : notably trigeminal neuralgia (ICHD-3 13.1), defined by unilateral painful paroxysms in the trigeminal territory, lasting from a few fractions of a second to 2 minutes, severe, lightning-like / electric shock-like, triggered by innocuous stimuli. The distinction from myogenous TMD is crucial because treatment differs radically (anticonvulsants, microvascular decompression vs conservative management).¹¹
• Otological conditions : otitis, Eustachian tube dysfunction.
• Pain of cervical origin : referred pain from the joints or muscles of the upper neck (cervicogenic headaches) can mimic TMD pain.¹²
• Systemic conditions : rheumatoid arthritis, fibromyalgia, which can have manifestations at the level of the TMJ.¹³

Should patients with temporomandibular disorders be classified, and for what benefits?

Absolutely. Classifying patients is the final objective of the diagnostic process and brings major benefits. The DC/TMD system offers a clear decision tree leading to specific diagnoses, mainly divided into three groups.¹,⁷

1. Muscle disorders : local myalgia, myofascial pain, myofascial pain with referral.
2. Disc displacements : disc displacement with reduction, disc displacement without reduction with limited opening, disc displacement without reduction without limited opening.
3. Joint disorders (arthralgia, osteoarthritis, headache) : arthralgia, TMJ osteoarthritis, headache attributed to TMD.

💡 The benefits of this precise classification are manifold:

• Targeted treatment direction : treating myalgia (physiotherapy, stress management) is fundamentally different from treating disc displacement without reduction with limited opening (specific manual therapy, education).¹⁴ Classification avoids an ineffective "one-size-fits-all" approach.
• Improved prognosis : understanding the exact nature of the disorder makes it possible to better predict its course. For example, a simple painless click has an excellent prognosis and often requires no intervention, whereas TMJ osteoarthritis may indicate a chronic degenerative condition.¹⁵
• Interprofessional communication : using standardised terminology (DC/TMD) facilitates communication between physiotherapists, dentists, maxillofacial surgeons and psychologists, ensuring coordinated care.⁴
• Inclusion in research : a homogeneous classification of patients is essential for conducting high-quality clinical trials and comparing the results of different studies, thus advancing knowledge about the most effective treatments.¹

Criticism and controversy

Despite its robustness, the DC/TMD model is not without challenges. One of the liveliest debates concerns the integration of Axis II into routine clinical practice. While its importance is unanimously recognised in research, many clinicians, through lack of time or training, focus almost exclusively on Axis I (the physical side).¹⁶ This purely biomedical approach is a major cause of treatment failure in patients with dominant psychosocial factors such as catastrophising or anxiety.

Another persistent controversy concerns the reliability of certain clinical tests. For example, palpation of the lateral pterygoid muscle, once considered a key test, is now judged unreliable and invalid because it is impossible to isolate this muscle from neighbouring structures.¹⁷ This underlines the importance of sticking to procedures validated by recent research.

Finally, the role of dental occlusion in the aetiology of TMD, once considered central, has been considerably relativised. Recent systematic reviews conclude that there is little solid evidence to support a cause-and-effect relationship between occlusal characteristics and the development of TMD, in favour of biopsychosocial factors.⁵,¹⁸ Yet many therapeutic approaches are still strongly focused on occlusal correction, creating a dichotomy between the scientific evidence and some clinical practices.

The management of temporomandibular disorders (TMD), a complex group of musculoskeletal and neuromuscular conditions affecting the temporomandibular joint (TMJ), the masticatory muscles and associated structures, rests on a multimodal, patient-centred approach. The recent scientific literature converges on a progressive model of care, favouring conservative, reversible and minimally invasive interventions as first-line management¹.

Where do you start? What is the recommended hierarchy of interventions?

The initial therapeutic approach for the majority of TMD is resolutely conservative. 💡 For chronic TMD pain (3 months or more), the BMJ practice guideline (Busse 2023), backed by a network meta-analysis (Yao 2023, 153 trials, 8,713 participants), recommends strongly, compared with placebo or a sham procedure: cognitive behavioural therapy with or without biofeedback or relaxation, therapist-assisted jaw mobilisation, manual trigger point therapy, supervised postural exercise, supervised jaw exercise and stretching, and usual care (home exercises, stretching, reassurance, education). It does not apply to acute pain.²¹,²² The Al-Moraissi 2020 network meta-analysis (48 randomised trials, more than 2,600 patients) had already found non-invasive interventions effective, without any one strategy standing out clearly from the others.² This philosophy is built around a clear hierarchy, starting with the interventions that are the least risky and the most empowering for the patient.

1. Therapeutic education and self-management: The foundation of any effective management is patient education³. This involves explaining the often benign and self-limiting nature of TMD, identifying and modifying parafunctions (such as tooth clenching, daytime bruxism, or chewing gum) and teaching stress management strategies⁴. This step aims to give the patient the tools to control their symptoms and prevent recurrences, which makes it the base of the care pyramid⁵.
2. Active therapies (exercise): Once the educational base has been established, active therapies, mainly therapeutic exercise, are introduced. They are considered a central intervention because of their capacity to improve function, reduce pain and promote patient autonomy⁶.
3. Passive therapies (manual therapy and modalities): Passive interventions, such as manual therapy and the use of technologies, are considered important adjuncts, especially when pain or mobility limitations hinder participation in active therapies⁷. Their role is often to "facilitate" the return to normal function, but they should not be the core of long-term treatment³.
4. Pharmacological interventions and appliances: Occlusal appliances (splints): the 2024 Cochrane review (57 trials, 2,846 participants) judges the certainty to be very low for all comparisons and does not allow a conclusion;²³ the 2023 BMJ guideline makes, for chronic pain, a conditional recommendation against reversible splints and a strong one against irreversible splints;²¹ the 2025 Japanese guideline retains the stabilisation appliance as a first-line option, on very low certainty.²⁴ The splint is not proscribed, but it is no longer presented as the demonstrated equivalent of education and exercise. Medications, such as non-steroidal anti-inflammatory drugs (NSAIDs), can be used for short-term pain management but do not treat the underlying cause⁸.

What is the place of exercise, and is there a superior approach?

Therapeutic exercise is a cornerstone of TMD treatment, with solid evidence supporting its effectiveness in reducing pain and improving mandibular range of motion and overall function¹⁹. A 2022 systematic review concluded that therapeutic exercises are particularly beneficial for TMD of muscular (myogenous) origin and that a clinician-supervised programme tends to give better results than an unsupervised one⁶. 🏋️‍♂️

There is no single universally superior type of exercise, but rather a combination of approaches adapted to the patient:

• Mobility and stretching exercises: They aim to restore a normal range of motion and reduce muscle stiffness. Controlled mouth-opening exercises and gentle stretching of the masticatory muscles are frequently prescribed¹⁰.
• Motor control and coordination exercises: These exercises, such as the "resting tongue position exercise" (tongue on the palate, teeth slightly apart, lips closed), help reprogramme dysfunctional motor patterns and reduce muscle tension at rest¹¹.
• Strengthening exercises: Light isometric and isotonic strengthening can be beneficial for improving the stability and endurance of the masticatory muscles, particularly in cases of hypermobility or joint instability⁶.

A meta-analysis has demonstrated that the combination of exercise therapy with manual therapy produces superior effects in terms of reducing pain intensity compared with exercise alone⁷. The most effective approach is therefore probably multimodal, integrating several types of exercise personalised according to the patient's TMD subtype.

Manual therapies, technologies: how effective are they really?

Manual therapies and physical modalities are valuable tools in the physiotherapist's armamentarium, mainly for managing symptoms in the short and medium term.

Manual therapy, which includes soft tissue and joint mobilisation techniques, has favourable effects, with a certainty that varies by technique. The Asquini 2022 systematic review (J Oral Rehabil), devoted specifically to craniomandibular manual therapy finds a beneficial effect on pain and mouth opening, despite very low quality of evidence linked to heterogeneity and small samples.¹² The integration of the cervical spine into treatment is now a matter of consensus: the Cuenca-Martínez 2020 meta-analysis (observational studies) confirms a clinically relevant association between cervical and mandibular disability in TMD patients (reduced pressure pain threshold and reduced cervical range of motion, moderate level of evidence). The Reynolds 2020 randomised trial (JOSPT, n = 50) added a high-velocity cervical manipulation, or a sham manipulation, to the educational programme, soft tissue techniques and exercises of TMD patients with myalgia: no difference in pain or mouth opening, earlier improvement in mandibular function and lower kinesiophobia at 4 weeks; the authors judge the additional effect of manipulation to be uncertain.¹³

Regarding technologies (electrophysiotherapy):

• Low-level laser therapy (LLLT) has been studied mainly in TMD of muscular origin (myalgia).¹⁴ The Xu 2018 meta-analysis (31 randomised trials) found it superior to placebo for short-term pain, with marked heterogeneity of parameters (wavelength, dose, duration).¹⁵ A 2025 network meta-analysis also finds an effect on pain, but of very low certainty, as for self-exercise and the splint;²⁵ the 2023 BMJ guideline makes, for chronic pain, a conditional recommendation against it,²¹ and the 2025 Japanese guideline a conditional recommendation for it, as a first-line option, on very low certainty.²⁴ It is an uncertain option, to be discussed with the patient, without delaying exercise or education.
• Therapeutic ultrasound and transcutaneous electrical nerve stimulation (TENS) are also used, but the evidence for their effectiveness is more mixed and often of lower quality than for LLLT or active approaches¹⁶.

In summary, manual therapy (assisted mobilisation, trigger points) is the subject of a strong recommendation in chronic pain (2023 BMJ guideline), as a complement to exercise, whereas LLLT remains an uncertain option. ✨

The certainty levels follow the BMJ network meta-analysis (Yao 2023), which judges the effect on pain of eight interventions, including CBT, assisted mobilisation, trigger points, supervised exercise and usual care, to be of moderate to high certainty; the other levels are an editorial judgement applying GRADE principles. The strength of recommendation (right-hand column) is a separate axis from certainty.

Beyond the physical: how do you educate the patient and act on psychological factors?

The biopsychosocial model is essential for understanding and treating TMD, because psychological factors such as anxiety, depression and stress are powerful modulators of chronic pain¹⁷. Complete management must therefore necessarily include an educational and behavioural component.

Education aims to:

• Demystify the condition: Reassuring the patient about the absence of serious pathology and explaining the physiology of pain can reduce fear and hypervigilance, factors that perpetuate pain¹⁸.
• Identify triggers: Helping the patient become aware of parafunctional habits (tooth clenching, jaw posture) is the first step towards changing them³.
• Promote self-efficacy: The aim is to make the patient an active participant in their recovery by providing simple self-management strategies (relaxation techniques, exercises, application of heat/cold)⁴.

acting on psychological factors does not mean that "the pain is all in the head", but recognises the interaction between stress and muscle tension. Approaches such as cognitive behavioural therapy (CBT) have shown their effectiveness in managing the chronic pain associated with TMD, by helping patients to change their thoughts and behaviours in response to pain¹⁹. Collaboration with psychologists or other mental health professionals may be indicated for patients with high levels of psychological distress²⁰.

Criticism and controversy

Despite a growing consensus on the conservative approach, several areas of debate persist. The most notable is the heterogeneity of TMD themselves. Classifying patients into subgroups (for example, arthralgia, myalgia, disc displacement) is crucial, because an intervention that is effective for one group may be ineffective for another. Future research should focus on stratified treatment protocols rather than on a single approach. Moreover, the long-term effectiveness of many passive modalities such as ultrasound remains questionable, raising the question of their relevance beyond acute pain management. Finally, the role and optimal type of occlusal appliance are the subject of continuing debate between the dental and physiotherapy professions, with the 2024 Cochrane review judging the certainty to be very low for all comparisons,²³ and the 2023 BMJ guideline conditionally recommending against reversible splints in chronic pain.²¹ The major challenge therefore remains to personalise treatment according to the patient's specific profile, integrating the physical, behavioural and psychological dimensions in a coherent way.

Sustaining the results obtained with manual therapy and preventing recurrences in temporomandibular disorders (TMD) rest on a successful transition from passive management to an active and autonomous strategy¹ This is a crucial phase in which the patient, armed with the right tools and knowledge, becomes the main guarantor of their long-term mandibular health. This approach, anchored in the biopsychosocial model, recognises that TMD are rarely a simple mechanical matter, but often a complex interaction between physical, psychological and social factors².

How do you make the patient an active participant in their recovery through self-management?

Self-management is the cornerstone of recurrence prevention in TMD³. It aims to give the patient the power (empowerment) to control their symptoms and maintain optimal mandibular function. 🧠 The effectiveness of this approach rests on several fundamental pillars identified by clinical research.

Firstly, therapeutic education is a sine qua non condition. A clear understanding of TMJ anatomy, pain mechanisms and aggravating factors makes it possible to defuse the condition and significantly improve adherence to exercise programmes⁴. Studies have shown that structured educational programmes, explaining in particular the role of parafunctions (such as bruxism or tooth clenching), are effective in reducing pain and the frequency of symptomatic episodes⁵. The aim is to replace erroneous beliefs with a functional understanding of the condition⁶.

Secondly, setting up a personalised home exercise programme is essential. Systematic reviews and meta-analyses confirm that a combination of mobilisation, motor control and strengthening exercises for the masticatory and cervical muscles reduces pain and improves functional capacity in a lasting way⁷,⁸. These exercises aim to restore normal mandibular kinematics and to strengthen the resilience of joint and muscle structures to everyday stresses⁹. A typical programme includes controlled opening, protrusion/retrusion and lateral movement exercises, performed without pain¹⁰.

Thirdly, management of parafunctions and lifestyle habits is a critical factor. The physiotherapist must help the patient identify and modify harmful behaviours: daytime tooth clenching, unilateral chewing, onychophagia (nail biting) or the maintenance of prolonged, unsuitable cervical postures¹¹. Biofeedback techniques or simple behavioural reminders can be integrated to automate new, healthier habits¹².

Finally, stress management and psychosocial factors must not be neglected. It has been shown that a high level of stress, anxiety or pain catastrophising are important predictors of the chronicity of TMD²,¹³. Integrating relaxation techniques, diaphragmatic breathing or mindful awareness (mindfulness) can significantly reduce hyperactivity of the masticatory muscles and improve pain perception¹⁴.

When and how should you plan a safe return to sport and activities?

Return to sport (RTS) or to demanding activities (for example, playing a wind instrument) after an episode of TMD should be gradual and guided by precise criteria rather than by a simple calendar. 💪 Although the scientific literature specific to RTS in TMD is less abundant than for other joints, the principles of sports rehabilitation apply fully¹⁵.

Planning the return to activities is built around a stepwise approach, based on achieving functional criteria:

• Phase 1: Pain control and restoration of basic function. The absolute prerequisite is the absence of pain during activities of daily living, including normal chewing and functional mouth opening (typically > 40 mm) without pain or apprehension⁷,⁹.
• Phase 2: Progressive reintroduction of loads. This phase consists of progressively re-exposing the TMJ to loads similar to those encountered in the targeted activity. For an athlete, this may mean resuming running (which generates vertical impacts) or wearing a mouthguard during light training¹⁶. For a musician, it will mean resuming short, low-intensity playing sessions. Monitoring symptoms 24 hours after exertion is crucial.
• Phase 3: Return to normal training and competition. Moving on to this phase is only possible if phase 2 has been completed without the reappearance of symptoms. The patient must have regained complete confidence in their jaw. Strengthening and motor control exercises must be maintained in the long term to prevent recurrences¹⁰.

The physiotherapist's role is to define functional tests specific to the patient's activity. For example, for a boxer, the ability to clench a mouthguard without pain during cardiovascular exertion is a relevant progression criterion. For a singer, the ability to maintain maximal mouth opening without pain for a defined duration may be an important milestone. 🎯

Criticism and controversy

Despite a growing consensus on the effectiveness of active approaches, several grey areas persist. A major controversy lies in the heterogeneity of TMD. Many clinical studies group together under the same diagnosis patients with very different profiles (myalgia, arthralgia, disc displacement), which can dilute the specific effects of the interventions. Future research should focus on stratified treatment protocols rather than on a single approach. Moreover, the long-term effectiveness of many passive modalities such as ultrasound remains questionable, raising the question of their relevance beyond acute pain management. Finally, the role and optimal type of occlusal appliance are the subject of continuing debate between the dental and physiotherapy professions, with the 2024 Cochrane review judging the certainty to be very low for all comparisons,²⁰ and the 2023 BMJ guideline conditionally recommending against reversible splints in chronic pain.²¹ The major challenge therefore remains to personalise treatment according to the patient's specific profile, integrating the physical, behavioural and psychological dimensions in a coherent way.

Temporomandibular disorders (TMD) represent a heterogeneous group of musculoskeletal and neuromuscular conditions involving the temporomandibular joint (TMJ), the masticatory muscles and associated structures¹. While systematic reviews and meta-analyses provide a high level of evidence on the effectiveness of treatments, clinical case studies offer invaluable insight into practical application, diagnostic challenges and the complexity of individualised management. 🧐 They illustrate the move from theory to clinical practice.

Analysis of a “classic” case: from assessment to resolution

The case study is a powerful teaching tool for understanding clinical reasoning in physiotherapy. The case reported by Lewis & Naude (2010, South African Journal of Physiotherapy) illustrates successful multimodal management in a man aged 26 years presenting simultaneously with cervicogenic headache and associated TMD. The protocol, spread over 9 physiotherapy sessions, combined several scientifically validated approaches²¹:

• Maitland manual therapy: cervical mobilisations (notably of the upper cervical spine) and of the TMJ to restore mobility and modulate pain.
• Soft tissue therapy: treatment of pain trigger sites (trigger points) and myofascial massage to reduce muscle tension.³
• Neuromuscular strengthening: work on the deep neck flexors and the scapulothoracic musculature.
• Postural reintegration: correction of craniocervical postural faults.

At the end of the programme, the patient showed a complete recovery of cervical and TMJ range of motion, improved muscle strength, and a significant reduction in the frequency and intensity of headaches on the reported outcomes (mobility measures, headache impact scales).²¹

This individual trajectory is consistent with the aggregated evidence from systematic reviews: the Armijo-Olivo 2016 meta-analysis finds clinically significant effects of the combination of manual therapy + exercise on pain and mouth opening in TMD patients⁴; in the Calixtre 2019 randomised trial, in 61 women with TMD, a 5-week protocol centred on the cervical spine (without any intra-oral procedure) significantly reduced orofacial pain and headache impact. The individual case nevertheless remains a low level of evidence: it illustrates without demonstrating.

The diagnostic challenge: when temporomandibular joint (TMJ) syndrome mimics another condition

One of the greatest lessons from clinical cases is the ability of TMD to present with symptoms that mimic other conditions, leading to diagnostic delays and ineffective treatments. ⚠️ The complex anatomical location of the TMJ and its neurological connections with the trigeminal nerve explain these atypical presentations.

The symmetry is in fact bidirectional: TMD can mimic other conditions, but other conditions can also mimic TMD. Several published and verifiable cases illustrate this diagnostic risk:

• 🔍 Eagle syndrome (elongated styloid process) mimicking TMD – Thoenissen et al. (2015, Int J Surg Case Rep) report the case of a 66-year-old man who had suffered for more than ten years from pain in the head, neck and shoulders, seen by several specialists and operated on for a cervical disc herniation without relief; the panoramic radiograph and then the scan showed styloid processes of 8.8 and 6.8 cm, and resection of a 4 cm fragment of the right process resolved the pain. The authors point out that this syndrome is easily confused with TMD and that a panoramic radiograph and an ultrasound are often enough to rule it out. Classic Eagle criteria: pain on cervical rotation, dysphagia, otalgia, foreign-body sensation in the pharynx. CT scan = diagnostic gold standard.¹⁵
• 🔍 Trigeminal neuralgia (ICHD-3 13.1) – the Maarbjerg/Cruccu 2017 review (Cephalalgia) stresses that confusion with TMD persists in practice despite distinct criteria: trigeminal neuralgia is characterised by lightning-like paroxysms, electric shock-like, lasting < 2 minutes, triggered by innocuous stimuli (touch, chewing, speech), unilateral and strictly within the trigeminal territory. Treatment (carbamazepine first-line, vascular decompression second-line) is radically different.⁵
• 🔍 Intramuscular pterygoid mass mimicking TMD – a 2024 case (Cureus) reports a 36-year-old patient with chronic TMJ pain and restricted opening resistant to conservative treatment, in whom MRI finally revealed a mass in the lateral pterygoid muscle. Any TMD that is resistant to 3-6 months of well-conducted conservative treatment should prompt a reconsideration of the diagnosis and consideration of advanced imaging.¹⁶
• 🔍 Abscesses of the facial fascial spaces disguised as TMD – Kim and Lee (2024) describe 3 abscesses of the fascial spaces, probably of dental origin, initially mistaken for TMD, with a potentially serious diagnostic delay. Very limited mouth opening (less than 15 mm), facial swelling or breathing difficulty are the warning signs that must immediately prompt a rethink.¹⁷

Likewise, otological symptoms (related to the ear) are frequent mimics. The reference study by Tuz et al. (n = 200 TMD patients vs controls) quantified this prevalence: 77.5% of TMD patients report at least one otological complaint (otalgia, tinnitus, vertigo, sensation of a blocked ear), versus a very low frequency in subjects without TMD.⁶ The Stechman-Neto 2016 systematic review also shows that conservative management of TMD (splint, advice, exercises) often leads to a partial or complete reduction of these otological signs, which supports the functional TMJ-ear link via anatomical proximity and trigeminal innervation.⁷ These data underline the importance of systematically including examination of the masticatory system in the differential diagnosis of craniofacial pain and unexplained otalgia; ENT / physiotherapist / dentist collaboration then becomes the key.

Study of a complex case

TMD are only rarely an isolated problem. They are often part of a broader clinical picture, involving comorbidities that complicate both diagnosis and treatment. Complex cases teach us the need for a biopsychosocial, multidisciplinary approach.

The link between the cervical spine and the TMJ is a classic example of complexity. The Calixtre 2019 randomised trial (J Oral Rehabil) showed that upper cervical mobilisation combined with deep craniocervical flexor training significantly improves orofacial pain, mandibular function and headaches in women with TMD, independently of any intra-oral procedure. Clinically, this supports current recommendations: treatment cannot be limited to the jaw but must target both regions as a functional unit, in line with the trigemino-cervical convergences at brainstem level. The Cuenca-Martínez 2020 meta-analysis (16 observational studies) confirms a robust association between cervical disability and TMD, in particular for pressure pain thresholds and cervical mobility.⁸

Complexity increases further in the presence of generalised pain conditions or central sensitisation. The Yakkaphan 2023 meta-analysis quantifies this overlap: 76.8% of fibromyalgia patients have TMD (essentially myogenous forms: 63%), and conversely 32.7% of TMD patients have comorbid fibromyalgia. In these patients, a purely biomechanical approach is doomed to failure.⁹ The strategy must integrate components of the biopsychosocial approach:

• Pain education: Explaining the mechanisms of central pain to defuse the symptoms and empower the patient (patient empowerment)⁹.
• Stress and anxiety management: Anxiety and catastrophising are major factors in maintaining pain in TMD¹⁰.
• Graded exercise: A gentle and progressive exercise programme to avoid the painful flare-ups typical of fibromyalgia.

Finally, bruxism (grinding or clenching of the teeth) is a frequent comorbidity that complicates management. Although it is a well-known risk and aggravating factor, its treatment is a challenge¹¹. Clinical cases show that an occlusal splint alone is often insufficient and that collaboration between dentist, physiotherapist and sometimes psychologist is necessary to manage the muscular and behavioural components of bruxism.

And in children? The particular case of juvenile idiopathic arthritis (JIA)

A paediatric situation deserves particular attention: juvenile idiopathic arthritis (JIA) can present with TMJ involvement as the only initial expression of the disease, with frequent diagnostic delay.¹⁸ The Ronsivalle 2024 meta-analysis (J Oral Rehabil, 366 children with JIA assessed by DC/TMD) finds a relative risk of TMD multiplied by 3.86 (95% CI 2.59–5.76) in children with JIA vs controls.¹⁹ Clinical symptoms may appear after significant condylar lesions are already established, hence the importance of early imaging (MRI) in any child with persistent TMJ involvement, especially with a rheumatological context or facial asymmetry.¹⁸

Key point: any child or adolescent with TMJ pain associated with progressive limitation of opening, mandibular asymmetry or hemifacial growth delay must undergo a rheumatological examination. A paediatric adaptation of the DC/TMD has been published (Rongo et al. 2021/2022) to provide specific tools for assessing under-18s.²⁰

Criticism and controversy: where do clinical cases sit in the hierarchy of evidence?

While clinical cases are enlightening, it is crucial to recognise their limitations and the controversies they raise. 🧠 The main criticism is their low level of evidence in the pyramid of scientific evidence. A single case illustrates a possibility, not a generality. It is impossible to conclude a cause-and-effect relationship, because placebo effects, regression to the mean or the natural history of the disease are not controlled¹². Moreover, published cases often tend to report successes, introducing a publication bias that can overestimate the effectiveness of an intervention.

A major controversy in the field of TMD is causality in the relationship between posture, the cervical spine and the jaw. The case of TMD with cervicogenic headache⁸ illustrates a strong association, but the debate persists: is it cervical dysfunction that causes TMD, the reverse, or do they share common risk factors? The literature does not yet settle the matter definitively¹³.

Finally, the heterogeneity of TMD, well classified by the Diagnostic Criteria for TMD (DC/TMD)¹⁴, makes generalisation from a single case perilous. A treatment that is effective for TMD of muscular origin (myalgia) may be unsuitable for a non-reducible disc displacement. Clinical cases, if they are not interpreted with caution and in the light of higher-level evidence, risk promoting "one-size-fits-all" approaches for a condition that, on the contrary, demands a precise stratification of patients.

Applying the recommendations from research is the bridge between science and improved patient outcomes. This requires not only knowing what to do, but also how to integrate it, when to collaborate and how to measure the impact. This section provides a practical framework for translating evidence into daily clinical action. 🧑‍⚕️

When, and to which other healthcare professionals, should you refer?

One of the fundamental skills of the modern physiotherapist is to recognise the limits of their scope of practice and to identify situations requiring interprofessional collaboration. This triage process is crucial for the safety and effectiveness of care.

The identification of "red flags" is the first non-negotiable step. These signs and symptoms suggest a serious underlying pathology (for example, a fracture, an infection, a tumour or cauda equina syndrome) and require immediate or emergency medical referral.¹ It is, however, crucial to note that many traditional red flags, taken in isolation, have low diagnostic accuracy and must be interpreted in the context of a complete clinical examination.² An international systematic review has also been published to establish a reference framework on red flags for potentially serious spinal pathologies.¹

Beyond emergencies, referral should be considered when the patient's problems go beyond the musculoskeletal scope of competence. The presence of "yellow flags", such as catastrophising beliefs, fear of movement or depressive symptoms, is a powerful predictor of chronic pain and disability.⁹ In these cases, collaboration with, or referral to, a psychologist, a pain management specialist or a general practitioner is strongly indicated for complete bio-psycho-social management.¹²

Finally, the growing complexity of healthcare favours interprofessional collaboration 🤝 in a structured way. The physiotherapist, often on the front line, plays a central role in the triage of patients within primary care teams.³ Clear communication and defined referral protocols with general practitioners, rheumatologists, orthopaedic surgeons and other specialists make it possible to optimise the patient's care pathway and to avoid diagnostic delays.³٬¹⁴ Advanced-practice physiotherapists, for example, are trained to assess, diagnose and manage complex cases, including prescribing imaging or referring directly to a surgeon, which streamlines the whole process.⁴

How do you measure outcomes and overcome barriers to implementation?

To ensure that interventions are effective, it is essential to measure outcomes objectively and in a standardised way. The systematic use of patient-reported outcome measures (PROMs) has become a standard for assessing the impact of treatments on pain, function and quality of life from the patient's point of view.⁶ However, their implementation runs up against significant obstacles, the most often cited being lack of time, technical difficulties with software and a lack of training in interpreting the results.⁶

To standardise this measurement on a larger scale, the scientific community is promoting the adoption of "Core Outcome Sets" (COS). This is an internationally agreed set of core outcome measures for a specific condition, ensuring that all clinicians and researchers assess the same critical domains.⁸ The use of COS allows more reliable comparisons between studies and better aggregation of data.⁸

Overcoming barriers to the implementation of evidence-based practice (EBP) is a major challenge. A 2022 systematic review identified the most common barriers perceived by physiotherapists: lack of time, lack of research skills and lack of support from the organisation.⁵ Key facilitators include strong leadership, access to resources (databases, dedicated time) and participation in continuing education.⁵٬¹⁵ The integration of shared decision-making is also a powerful lever, although its implementation is itself hampered by perceived lack of time and clinicians' need for training.⁷ It is a collaborative process in which clinician and patient make healthcare decisions together, taking into account the best available evidence as well as the patient's values and preferences.¹³ 📊

Strategies to overcome these barriers 🚧 must be multi-faceted, combining solutions at the individual level (training, mentoring), organisational level (protected time, access to resources) and systemic level (health policies favouring EBP).¹⁵ The "de-implementation" of low-value practices, such as the use of certain passive modalities without supporting evidence, is just as important but runs up against barriers such as patient expectations or practitioners' habits.¹⁷

Criticism and controversies: beyond the guidelines

While guidelines offer a reassuring framework, their rigid application can mask important complexities and controversies in clinical practice.

Firstly, the red flag paradox. While looking for them is imperative for safety, the scientific literature has shown that most individual red flags have a very low positive predictive value for serious pathology.² This reality places the clinician in a delicate position: they must remain vigilant without over-medicalising benign presentations. True competence does not lie in memorising a list, but in the ability to group signs together, recognise patterns and use probabilistic clinical reasoning, a skill that is much harder to standardise.¹

Secondly, the persistent gap between knowledge and practice ("knowing-doing gap"). We have had robust systematic reviews on barriers to implementation for years.⁵٬¹⁵ Yet the same obstacles (lack of time, skills, support) are consistently reported. This suggests that the problem may not be a lack of knowledge about "how to do it", but rather a systemic and cultural problem within healthcare organisations. The move to evidence-based practice may require a deeper overhaul of economic models, working structures and initial training, rather than mere "knowledge translation" interventions.

Thirdly, standardisation versus personalisation. The rise of "Core Outcome Sets"⁸ and standardised care pathways (clinical pathways) is essential for research and quality of care. However, there is a tension with the increasingly personalised, patient-centred approach. How can the use of a standardised questionnaire be reconciled with a patient's unique and specific goals, which are not necessarily captured by this tool? Expert practice consists of navigating between these two poles: using standardised tools for follow-up and communication, while carrying out an individualised assessment that guides tailor-made therapy. This is the art of clinical science.