Temporomandibular disorders (TMD) is a collective term for a group of musculoskeletal conditions involving pain and/or dysfunction in the masticatory muscles, temporomandibular joints (TMJ) and associated structures. It is the most common type of non-odontogenic orofacial pain and patients can present with pain affecting the face/head, TMJ and/or teeth, limitations in jaw movement and sounds in the TMJ during jaw movements. Comorbid painful and non-painful conditions are also common among individuals with TMD. The diagnosis of TMD have significantly improved over time with the recent Diagnostic Criteria for TMD (DC/TMD) being reliable and valid for most common diagnoses, and an efficient way to communicate in multidisciplinary settings. This classification covers 12 most common TMD, including painful (myalgia, arthralgia and headache attributed to TMD) as well as the non-painful (disc displacements, degenerative joint disease and subluxation) TMD diagnoses. Recent studies have demonstrated that the pathophysiology of common painful TMD is biopsychosocial and multifactorial, where no one factor is responsible for its development. Importantly, research has suggested different predisposing, initiating and perpetuating factors, including both peripheral and central mechanisms. This is an active field of investigation and future studies will not only seek to clarify specific causal pathways but translate this knowledge into mechanism-directed diagnosis and treatment. In accordance with this complex aetiology, current evidence supports primarily conservative multidisciplinary treatment including self-management strategies, behavioural therapy, physical therapy and pharmacotherapy. The aim of this review is to present an overview of most recent developments in aetiology, pathophysiology, diagnosis and management of TMD.

Background Quantification of motor‐evoked potentials (MEPs) can contribute to better elucidate the central modulation of motor pathways in response to nociceptive inputs. The primary aim of this study was to assess the modulatory effects of nerve growth factor (NGF) injection on masseter corticomotor excitability. Methods The healthy participants of this randomized, double blind placebo‐controlled experiment were assigned to have injected into the right masseter muscle either NGF (n = 25) or isotonic saline (IS, n = 17). The following variables were assessed at baseline and 48 hr after the injection: right masseter MEP amplitude and corticomotor mapping and clinical assessment of jaw pain intensity and function. Repeated Measures ANOVA was applied to the data. Results NGF caused jaw pain and increased jaw functional disability after the injection (p < 0.050). Also, the participants in the NGF group decreased the MEP amplitude (p < 0.001) but the IS group did not present any significant modulation after the injection (p > 0.050). Likewise, the participants in the NGF group reduced corticomotor map area and volume (p < 0.001), but the IS group did not show any significant corticomotor mapping changes after the injection (p > 0.050). Finally, there was a significant correlation between the magnitude of decreased corticomotor excitability and jaw pain intensity on chewing 48 hr after the NGF injection (r = −0.51, p = 0.009). Conclusion NGF‐induced masseter muscle soreness can significantly reduce jaw muscle corticomotor excitability, which in turn is associated with lower jaw pain intensity and substantiates the occurrence of central changes that most likely aim to protect the musculoskeletal orofacial structures. Significance Intramuscular administration of nerve growth factor into masseter muscle causes inhibitory corticomotor plasticity, which likely occurs to prevent further damage and seems associated with lower pain intensity on function.

These findings support the idea that mechanical sensitization in the masseter and temporalis muscles differs following injections of nerve growth factor. Furthermore, referred pain and headache frequency do not seem to be related to nerve growth factor sensitization in this model. These findings support the idea that in healthy individuals referred pain may be an epiphenomenon of the muscle in response to noxious input.

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Referred sensations (RS) are commonly found in various musculoskeletal pain conditions. Experimental studies have shown that RS can be elicited through glutamate injection and mechanical stimulation. Despite this, differences and similarities between these modalities in RS outcomes remain unclear. The aim of this study was to assess differences between mechanical-induced and glutamate injection-induced RS in the trigeminal region. The present randomized, double-blind, controlled, cross-over study recruited 60 healthy participants who were assessed in 2 different sessions. In both sessions, pressure was applied to the masseter muscle with 4 different forces (0.5, 1, 2, and 4 kg), and glutamate (1 mol/L or 0.25 mol/L) was injected into the same area. Participants rated their perceived masseter sensations and rated and drew any RS they experienced. No difference was found in number of participants reporting RS after glutamate injection compared with mechanical stimulation. More participants reported RS when the stimulus was painful compared with a nonpainful stimulus. Furthermore, it was shown that the more intense the stimulus, the higher the frequency of RS. Finally, RS centre-of-gravity location was similar between the 2 sessions. In summary, RS was elicited in healthy individuals through both modalities, and no differences in frequency of RS were observed in the orofacial region. Hence, RS does not seem to be modality-dependent, and only the painfulness of the stimulus caused an increase in frequency of RS. Finally, RS location for each participant was similar in both sessions possibly indicating a preferred location of referral. These findings may have implications for our understanding of RS in craniofacial pain conditions.