Nerve Growth Factor-Induced Sensitization of the Sternocleidomastoid Muscle and Its Effects on Trigeminal Muscle Sensitivity and Pain Profiles: A Randomized Double-Blind Controlled Study.

AIMS: To investigate whether localized sensitization of the sternocleidomastoid (SCM) muscle using nerve growth factor (NGF) would affect masseter and anterior temporalis muscle sensitivity and pain profiles. METHODS: A total of 28 healthy participants attended two sessions (T0 and T1). At T0, the maximum voluntary occlusal bite force (MVOBF), as well as pressure pain thresholds (PPT), mechanical sensitivity, and referred pain/sensations for the SCM, masseter, and temporalis muscles, were assessed. Participants also completed the Pain Catastrophizing Scale (PCS), the Pain Vigilance and Awareness Questionnaire (PVAQ), and the Neck Disability Index (NDI). After these assessments, 14 participants received an injection of NGF into the SCM, and 14 received an injection of isotonic saline solution. At T1 (48 hours postinjection), the participants were again submitted to the same evaluations. RESULTS: NGF caused significant mechanical sensitization in the SCM (P < .025), but not in the masseter or temporalis muscles (P > .208). It also caused significant increases in NDI score (P = .004). No statistically significant differences were found for MVOBF, frequency of referred pain/sensations, or questionnaire scores (P > .248). CONCLUSION: These results suggest that 48 hours after localized sensitization of the SCM, the primary response is impairment of neck function, but not jaw function.

Temporomandibular disorders: a review of current concepts in aetiology, diagnosis and management.

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.

Characterization and predictive mechanisms of experimentally induced tension-type headache.

OBJECTIVE: Studies have shown it is possible to elicit a tension-type headache episode in 15 to 30% of healthy individuals following a tooth-clenching or stress-inducing task. Despite this, no studies have attempted to understand why some healthy individuals develop a headache episode while others do not. METHODS: The present randomized, single-blind, controlled study recruited 60 healthy participants who participated in a 30-minute tooth-clenching task and 10 participants who participated in a control task. Before the tasks, participants had their pericranial tenderness and pain modulation profiles (wind-up ratio and conditioned pain modulation) assessed. Two hours later, pericranial tenderness and pressure pain thresholds were assessed as well as any developing temporomandibular disorders. Pain diaries were kept for 24 hours to register any developing pain or headache. RESULTS: Participants with a decrease in pericranial tenderness after the tooth-clenching task were less likely to develop headache when compared to participants without. Pain modulation profiles could not predict who developed headache and who did not. Finally, no difference was found between groups for developing temporomandibular disorders. No difference in frequency of participants who developed headache was found between the tooth-clenching and the control task. CONCLUSIONS: In conclusion, it was shown that increased pericranial tenderness was not required to trigger an episode of tension-type headache in healthy participants. Furthermore, pain modulation profiles could not predict who developed headache and who did not. Finally, activation of descending inhibitory pathways, as assessed by decreases in pericranial tenderness, was protective against the development of headache. These findings provide new insights into the pathophysiology of experimentally-induced tension-type headache.