The link between cutaneous allodynia and pain/sensitivity in teeth and gums during migraine episodes.

BACKGROUND: Migraine is one of the most common primary headaches worldwide, while toothache is the most common pain in the orofacial region. The association of migraine pain, and oral pain is unknown. This study aims to investigate the association between migraine and dental and gingival pain with the presence of allodynia. METHODS: A questionnaire comprising demographic data with the ID-Migraine (IDM) tool, an Allodynia Symptom Checklist (ASC), and inquiries about pain and sensitivity in the teeth and gums during migraine attacks was administered to the participants and 762 responded the survey. The study classified participants based on the ASC, and the relationship between allodynia and pain/sensitivity in the teeth and/or gums during migraine attacks was analyzed. The statistical analyses utilized Chi-square tests and the Fisher-Exact test. RESULTS: Among 762 migraine patients, 430 (56.44%) were classified as allodynia (+), while 332 (43.56%) were classified as allodynia (-) (p < 0.001). Additionally, 285 participants (37.5%) reported experiencing pain and sensitivity in the teeth and gums during migraine attacks, with a significant relationship observed between allodynia and pain/sensitivity in the teeth and/or gums during migraine attacks (p < 0.001). CONCLUSION: The findings of this study have important clinical implications. For migraine patients who are non-allodynic, the presence of pain and sensitivity in their teeth and gums during migraine attacks may indicate underlying dental diseases or the need for dental treatment especially root canal treatment. However, for allodynic patients, such symptoms may not necessarily indicate the presence of dental diseases or the need for dental treatment especially root canal treatment. These results underscore the significance of considering the presence of allodynia in the assessment and management of oral symptoms during migraine attacks.

Systemic Factors Affecting Pain Management in Dentistry.

There are several factors that affect a patient's experience of pain. These include both local and systemic factors. The systemic factors that affect patients' dental and orofacial pain experience include, but not limited to, hormonal, nutritional, systemic infections, neurodegenerative, and autoimmune, among others. Comprehensive medical history is essential to delineate any possible systemic factors affecting pain experience. A thorough review of systems should form the foundation, since multiple factors can affect the prognosis of pain management. This would facilitate early recognition and trigger prompt referrals to the appropriate medical professionals. This helps to reduce the health care burden.

Treatment of temporomandibular joint internal derangement using MESNA injection.

INTRODUCTION: The development of temporomandibular disorders specifically emphasizes the biochemical changes occurring in the synovial fluid at different stages of temporomandibular joint disease. Research has indicated that inflammation may be a primary reason behind the pain and dysfunction in temporomandibular joint diseases. Since its clearance several years ago, MESNA (sodium 2-mercaptoethanesulfonate) has been used in various formulations as a mucolytic drug in the respiratory domain. It operates by disrupting the disulfide bonds present between polypeptide chains within mucus. MESNA exhibits minimal tissue distribution, with the material being swiftly and thoroughly eliminated via the kidneys. OBJECTIVES: To assess the efficacy of injecting MESNA directly into the Temporomandibular Joint to treat internal derangement. MATERIALS AND METHODS: A randomized clinical trial was conducted on sixty patients who exhibited non-responsiveness to conventional treatment and were diagnosed with TMJ anterior disc displacement with reduction. The patients were chosen from the outpatient clinic of the Oral and Maxillofacial Surgery Department at Tanta University Faculty of Dentistry. Two equal groups of patients were randomly assigned to each other. Group I (Mesna group) received intra-articular injection with MESNA solution. Group II (Standard group) received arthrocentesis with lactated ringer solution followed by injection of Hyaluronic Acid (HA). The data was gathered by functional examinations such as maximum interincisal opening (MIO) and clicking. A Visual Analogue Scale (VAS) assessed pain severity before and after treatments. RESULTS: Both MESNA and HA showed significant improvement up to six months of the follow-up compared to preoperative status, as evidenced by better mouth opening, lateral excursion, lower clicking, and reduced pain score in patients with TMDs. MESNA showed significant improvement during follow-up compared to HA. CONCLUSION: Compared to HA, MESNA showed a more noticeable improvement during the follow-up period.

Clinical profile in relation to age and gender of patients with temporomandibular disorders: a retrospective study.

BACKGROUND: The present study is to evaluate the clinical characteristics of patients with temporomandibular disorders (TMD). METHODS: A total of 3362 TMD patients were included. Each participant had complete medical records according to the diagnostic criteria for temporomandibular disorders (DC/TMD). The clinical characteristics including symptoms and signs in relation to age and gender were analyzed. RESULTS: The mean age of the patients seeking care was 29.89 ± 13.73Y, and 68.6% of patients were aged 16-35 years. The female-to-male ratio of patients was 2.2: 1, and the average age of males was significantly lower than that of females. The prevalence of clicking symptoms decreased with age, while the prevalence of pain symptoms and limitations in jaw movement increased with age. Females were more likely to have limitations in jaw movement than males. Among the patients with pain, the average visual analogue scale (VAS) was 2.96 ± 1.23. The average VAS score of acute TMD patients (≤ 3 months) was significantly higher than that of chronic TMD patients (> 3 months). CONCLUSIONS: The majority of TMD patients seeking care were young people. The number and average age of female patients was higher than the males. Female patients were more likely to have limitations in jaw movement than males.

[28-year-old male patient with headaches on the left side and facial pain]. / 28-jähriger Patient mit in den Kiefer ausstrahlenden ­Kopfschmerzen temporal links.

INTRODUCTION: A 28-year-old male suffers for two weeks from new-onset very severe headache located on his left temple radiating to his jaw. He also complains about left sided retroorbital pain and chewing aggravated symptoms. In addition, nausea and emesis in the mornings during the past six months were reported. Clinical examination revealed tender swelling over the left temple, but laboratory results showed no signs of inflammation, normal electrolytes, kidney and liver values. A CT-scan revealed a circumscriptive osteolytic lesion in the left os temporale.

A Case Report on Unstable Angina Pectoris Manifesting as Orofacial Pain.

Cardiac ischemia, such as angina pectoris or myocardial infarction, is associated with pain in the oral cavity, lower jaw, head, or neck, or spanning from the left upper arm to the shoulder. When presenting to a dentist, however, appropriate treatment for such patients is often delayed, as dental problems are usually the first to be suspected when the chief complaint is orofacial pain. This report describes a case of a 70-year-old woman who was aware of pain and a burning sensation in the oral cavity upon exertion for a year prior to presenting at our clinic. She had been examined by her family physician, an otolaryngologist, and another dentist, none of whom found any abnormalities other than suspected periodontal disease and caries, for which she was treated. An examination at our clinic revealed no abnormal dental findings that would have been consistent with the mandibular pain, however. Although no chest symptoms were reported, pain was elicited on exertion, suggesting cardiogenic toothache. An immediate referral to a cardiologist was therefore made on the same day. The patient visited the cardiology department of the University Hospital of Tokyo Dental College 6 days later. The increased frequency of symptoms on exertion suggested unstable angina, and the patient was admitted to the emergency department on the same day. Emergency coronary angiography showed that right coronary artery #1 was 99% stenosed proximally (highly calcified plaque). The diagnosis was unstable angina pectoris, with the right coronary artery #1 as the responsible lesion, and percutaneous coronary angioplasty was performed on the same day. Subsequently, all the orofacial pain disappeared, confirming unstable angina as the cause. The pain characteristics in this case were consistent with pain associated with cardiac ischemia, which led to the immediate referral to the cardiology department. In cases of toothache associated with cardia ischemia, it is essential to seek cardiological care as soon as possible.

Orofacial antinociceptive activity of codeine-associated geraniol in mice: a controlled triple-blind study.

This is a nonclinical, controlled, and triple-blind study to investigate the effects of codeine-associated geraniol on the modulation of orofacial nociception and its potential central nervous system depressing effect in an animal model. The orofacial antinociceptive activity of geraniol in combination with codeine was assessed through the following tests: (i) formalin-induced pain, (ii) glutamate-induced pain, and (iii) capsaicin-induced pain. Six animals were equally distributed into six groups and received the following treatments, given intraperitoneally (i.p.) 30 minutes before the experiments: a) geraniol/codeine 50/30 mg/kg; b) geraniol/codeine 50/15 mg/kg; c) geraniol/codeine 50/7.5 mg/kg; d) geraniol 50 mg/kg; e) codeine 30 mg/kg (positive control); or f) 0.9% sodium chloride (negative control). We performed pain behavior analysis after the injection of formalin (20 µL, 20%), glutamate (20 µL, 25 µM), and capsaicin (20 µL, 2.5 µg) into the paranasal region. Rubbing time of the paranasal region by the hind or front paw was used as a parameter. In the neurogenic phase of the formalin test, the geraniol/codeine at 50/7.5 mg/kg was able to promote the maximum antinociceptive effect, reducing nociception by 71.9% (p < 0.0001). In the inflammatory phase of the formalin test, geraniol/codeine at 50/30 mg/kg significantly reduced orofacial nociception (p < 0.005). In the glutamate test, geraniol/codeine at 50/30 mg/kg reduced the rubbing time by 54.2% and reduced nociception in the capsaicin test by 66.7% (p < 0.005). Geraniol alone or in combination does not promote nonspecific depressing effects on the central nervous system. Based on our findings, we suggest the possible synergy between geraniol and codeine in the modulation of orofacial pain.

Impact of streptozotocin-induced diabetes on experimental masseter pain in rats.

This study aimed to assess the influence of streptozotocin (STZ)-induced diabetes on the nociceptive behavior evoked by the injection of hypertonic saline (HS) into the masseter muscle of rats. Forty male rats were equally divided into four groups: a) isotonic saline control, which received 0.9% isotonic saline (IS), (Ctrl-IS); b) hypertonic saline control, which received 5% HS (Ctrl-HS); c) STZ-induced diabetic, which received IS, (STZ-IS); d) STZ-induced diabetic, which received HS (STZ-HS). Experimental diabetes was induced by a single intraperitoneal injection of STZ at dose of 60 mg/kg dissolved in 0.1 M citrate buffer, and 100 µL of HS or IS were injected into the left masseter to measure the nociceptive behavior. Later on, muscle RNA was extracted to measure the relative expression of the following cytokines: cyclooxygenase-2 (COX-2), tumor necrosis factor (TNF-α), and interleukins (IL)-1ß, -2, -6, and -10. One-way analysis of variance (ANOVA) was applied to the data (p < 0.050). We observed a main effect of group on the nociceptive response (ANOVA: F = 11.60, p < 0.001), where the Ctrl-HS group presented the highest response (p < 0.001). However, nociceptive response was similar among the Ctrl-IS, STZ-IS, and STZ-HS group (p > 0.050). In addition, the highest relative gene expression of TNF-α and IL-6 was found in the masseter of control rats following experimental muscle pain (p < 0.050). In conclusion, the loss of somatosensory function can be observed in deep orofacial tissues of STZ-induced diabetic rats.

High prevalence of orofacial pain in juvenile fibromyalgia as detected by a novel tool specifically devised for children and adolescents.

OBJECTIVES: To examine the prevalence of temporomandibular disorders (TMD) in patients with juvenile fibromyalgia syndrome (JFS) and identify TMD characteristics specifically associated to JFS. METHODS: Signs and symptoms of TMD were assessed using a novel clinical tool specifically devised for children that consists of: 1. a self-report multiple-choice questionnaire; 2. a protocol for the clinical examination of the orofacial region. Multivariate logistic regression model was used to identify TMD features associated with JFS. RESULTS: Thirty JFS patients (median age 15.5 years) and 45 healthy controls (median age 15.0 years) were included in this cross-sectional study. Orofacial pain was reported by 26 of 30 JFS patients (86.7%) and by 3 of 45 controls (6.7%; p<0.001). Pain on TMJ palpation was present in 18 of 30 JFS patients (60%) and in 5 of 45 controls (11.1%; p<0.001). Median values of maximum spontaneous mouth opening, voluntary active opening and assisted passive opening were significantly higher in JFS patients than in controls. On multiple regression analysis spontaneous orofacial pain (OR: 21.0; p=0.005), diffuse tenderness on palpation of the masticatory muscles (OR: 14.9; p=0.026) and TMJ hypermobility (OR 1.42; p=0.008) were independently associated with JFS. CONCLUSIONS: The high prevalence of TMD in JFS highlights the need for a broader interdisciplinary evaluation of JFS patients. TMJ hypermobility, in addition to orofacial and masticatory muscle pain, is an important clue for the diagnosis of TMD in adolescents with JFS. Elucidating the link between these disorders will advance individualised management and improve treatment efficacy.

Role of HDAC5 Epigenetics in Chronic Craniofacial Neuropathic Pain.

The information provided from the papers reviewed here about the role of epigenetics in chronic craniofacial neuropathic pain is critically important because epigenetic dysregulation during the development and maintenance of chronic neuropathic pain is not yet well characterized, particularly for craniofacial pain. We have noted that gene expression changes reported vary depending on the nerve injury model and the reported sample collection time point. At a truly chronic timepoint of 10 weeks in our model of chronic neuropathic pain, functional groupings of genes examined include those potentially contributing to anti-inflammation, nerve repair/regeneration, and nociception. Genes altered after treatment with the epigenetic modulator LMK235 are discussed. All of these differentials are key in working toward the development of diagnosis-targeted therapeutics and likely for the timing of when the treatment is provided. The emphasis on the relevance of time post-injury is reiterated here.

Cytoarchitecture and intercellular interactions in the trigeminal ganglion: Associations with neuropathic pain in the orofacial region.

BACKGROUND: Disorders of the trigeminal nerve, a sensory nerve of the orofacial region, often lead to complications in dental practice, including neuropathic pain, allodynia, and ectopic pain. Management of these complications requires an understanding of the cytoarchitecture of the trigeminal ganglion, where the cell bodies of the trigeminal nerve are located, and the mechanisms of cell-cell interactions. HIGHLIGHTS: In the trigeminal ganglion, ganglion, satellite, Schwann, and immune cells coexist and interact. Cell-cell interactions are complex and occur through direct contact via gap junctions or through mediators such as adenosine triphosphate, nitric oxide, peptides, and cytokines. Interactions between the nervous and immune systems within the trigeminal ganglion may have neuroprotective effects during nerve injury or may exacerbate inflammation and produce chronic pain. Under pathological conditions of the trigeminal nerve, cell-cell interactions can cause allodynia and ectopic pain. Although cell-cell interactions that occur via mediators can act at some distance, they are more effective when the cells are close together. Therefore, information on the three-dimensional topography of trigeminal ganglion cells is essential for understanding the pathophysiology of ectopic pain. CONCLUSIONS: A three-dimensional map of the somatotopic localization of trigeminal ganglion neurons revealed that ganglion cells innervating distant orofacial regions are often apposed to each other, interacting with and potentially contributing to ectopic pain. Elucidation of the complex network of mediators and their receptors responsible for intercellular communication within the trigeminal ganglion is essential for understanding ectopic pain.

Non-neuronal cells act as crucial players in neuropathic orofacial pain.

BACKGROUND: Following peripheral nerve damage, various non-neuronal cells are activated, triggering accumulation in the peripheral and central nervous systems, and communicate with neurons. Evidence suggest that neuronal and non-neuronal cell communication is a critical mechanism of neuropathic pain; however, its detailed mechanisms in contributing to neuropathic orofacial pain development remain unclear. HIGHLIGHT: Neuronal and non-neuronal cell communication in the trigeminal ganglion (TG) is believed to cause neuronal hyperactivation following trigeminal nerve damage, resulting in neuropathic orofacial pain. Trigeminal nerve damage activates and accumulates non-neuronal cells, such as satellite cells and macrophages in the TG and microglia, astrocytes, and oligodendrocytes in the trigeminal spinal subnucleus caudalis (Vc) and upper cervical spinal cord (C1-C2). These non-neuronal cells release various molecules, contributing to the hyperactivation of TG, Vc, and C1-C2 nociceptive neurons. These hyperactive nociceptive neurons release molecules that enhance non-neuronal cell activation. This neuron and non-neuronal cell crosstalk causes hyperactivation of nociceptive neurons in the TG, Vc, and C1-C2. Here, we addressed previous and recent data on the contribution of neuronal and non-neuronal cell communication and its involvement in neuropathic orofacial pain development. CONCLUSION: Previous and recent data suggest that neuronal and non-neuronal cell communication in the TG, Vc, and C1-C2 is a key mechanism that causes neuropathic orofacial pain associated with trigeminal nerve damage.

Muscle oxygenation and pain in different types of temporomandibular disorders.

OBJECTIVES: Studies exploring variations in peripheral muscle oxygenation and pressure pain thresholds (PPT) of masticatory muscles in individuals with Temporomandibular Disorders (TMDs) are limited. The purpose of this study was to compare variations in peripheral oxygenation of the masseter muscle; PPT of the masseter and temporal muscles and correlate peripheral muscle oxygenation and PPT of the masseter muscle in individuals with different types of TMDs. MATERIALS AND METHODS: Cross-sectional study involving 116 participants classified into three groups: muscle group (MG, n = 32), joint group (JG, n = 30) and muscle-joint group (MJG, n = 54). Individuals aged 26.97 ± 6.93, 68.97% female, 31,03% males were included. All participants were evaluated using the Diagnostic Criteria for Temporomandibular Disorders, Near-infrared spectroscopy (NIRS) for peripheral muscle oxygenation and pressure algometer for PPT. RESULTS: There was no difference in masseter muscle oxygenation among groups. In the masseter muscle, a weakly positive correlation was observed between PPT and variation in tissue saturation index in the MG (rho = 0.365) and JG (rho = 0.317). In addition, the MJG expressed lower PPT (p = 0.004) than JG, demonstrating that MJG had more pain in this muscle. CONCLUSIONS: MJG have lower PPT in the masseter muscle. Although the PPT is dependent on the type of TMDs, the correlation between PPT and oxygenation is weak. All TMDs groups evaluated (MG, JG, MJG) showed hemodynamic similarities of the masseter muscle. CLINICAL RELEVANCE: Understanding pain thresholds and the hemodynamic behavior of the masticatory muscles contributes to a more assertive physiotherapeutic assessment in TMDs, serving as a basis for careful and individualized interventions.

Contribution of inwardly rectifying potassium channel 4.1 in orofacial neuropathic pain: Regulation of pannexin 3 via the reactive oxygen species-activated P38 MAPK signal pathway.

The involvement of inwardly rectifying potassium channel 4.1 (Kir4.1) in neuropathic pain has been established. However, there is limited understanding of the downstream mechanism through which Kir4.1 contributes to orofacial neuropathic pain. The objective of this study was to examine the regulation of Kir4.1 on the expression of pannexin 3 (Panx3) in the trigeminal ganglion (TG) and the underlying mechanism in the context of orofacial neuropathic pain caused by chronic constriction injury of the infraorbital nerve (CCI-ION). The study observed a significant increase in Panx3 expression in the TG of mice with CCI-ION. Inhibition of Panx3 in the TG of CCI-ION mice resulted in alleviation of orofacial mechanical allodynia. Furthermore, conditional knockdown (CKD) of Kir4.1 in the TG of both male and female mice led to mechanical allodynia and upregulation of Panx3 expression. Conversely, overexpression of Kir4.1 decreased Panx3 levels in the TG and relieved mechanical allodynia in CCI-ION mice. In addition, silencing Kir4.1 in satellite glial cells (SGCs) decreased Panx3 expression and increased the phosphorylation of P38 MAPK. Moreover, silencing Kir4.1 in SGCs increased the levels of reactive oxygen species (ROS). The elevated phosphorylation of P38 MAPK resulting from Kir4.1 silencing was inhibited by using a superoxide scavenger known as the tempol. Silencing Panx3 in the TG in vivo attenuated the mechanical allodynia caused by Kir4.1 CKD. In conclusion, these findings suggest that the reduction of Kir4.1 promotes the expression of Panx3 by activating the ROS-P38 MAPK signalling pathway, thus contributing to the development of orofacial neuropathic pain.

Modulatory Processes in Craniofacial Pain States.

Pain is a common symptom associated with many disorders affecting the craniofacial tissues that include the teeth and their supporting structures, the jaw, face and tongue muscles, and the temporomandibular joint. Most acute craniofacial pain states are easily recognized and readily treated, but chronic craniofacial pain states (e.g., temporomandibular disorders [TMD], trigeminal neuropathies, and some headaches) may be especially challenging to manage successfully. This chapter provides an overview of the processes that underlie craniofacial pain, with a focus on the pain-modulatory mechanisms operating in craniofacial tissues and in the central nervous system (CNS), including the role of endogenous chemical processes such as those involving opioids. The chapter outlines in particular findings from preclinical studies that have provided substantial information about the neural as well as nonneural (e.g., glial) processes involved in the initiation, transmission, and modulation of nociceptive signals in the trigeminal system, and also draws attention to their clinical correlates. The increased understanding gained from these preclinical studies of how nociceptive signals can be modulated will contribute to improvements in presently available therapeutic approaches to manage craniofacial pain as well as to the development of novel analgesic approaches.

Do symptoms and signs of temporomandibular disorders have an association with breathing pattern: a cross-sectional study on Turkish children and adolescents.

BACKGROUND: This paper aimed to explore the prevalence of temporomandibular disorders (TMDs) signs/symptoms, and to investigate the possible link between signs/symptoms of TMDs and mouth breathing (MB) by evaluating along with other risk factors, in a Turkish subpopulation of children and adolescence. METHODS: This study was conducted with the archival data of the patients who applied with orthodontic complaints. Data on demographic characteristics, family-related factors, systemic status, occlusion, breathing patterns, oral habits, and bruxism were retrieved from the archival records. RESULTS: Nine hundred forty-five children and adolescents with a mean age of 14.82 ± 2.06 years were included in the study. Of the participants, 66% were girls, 60.4% were delivered by C-section, 8.4% of the participants had at least one systemic disease, 9.2% of the participants had allergy, and 4.3% of the participants' parents were divorced, 18.7% have an oral habit, 6.6% have bruxism, 29.8% have malocclusion and 14.1% have MB. Eight-point-five percent of participants have signs/symptoms of TMD. Among them 2.9% have pain, 3.7% have joint sounds, 1.4% have deflection, and 3.9% have deviation. Evaluation of the risk factors revealed a significant relation between the signs/symptoms of TMD and bruxism (OR 8.07 95% CI 4.36-14.92), gender (OR 2.01 95% CI 1.13-3.59), marital status of parents (OR 2.62 95% CI 1.07-6.42), and MB (OR 3.26 95% CI 1.86-5.71). CONCLUSIONS: According to the study's findings, girls and those with bruxism, divorced parents, and MB behavior are more likely to have signs/symptoms of TMD. Age found to have significant effect on the occurrence of the signs/symptoms of TMD alone, but together with other factors the effect of the age is disappeared. Early screening and intervention of MB as well as the signs/symptoms of TMD can help to limit detrimental effects of these conditions on growth, and quality of life of children and adolescents.

Development of a novel three-dimensional injection guide for trigeminal ganglia.

BACKGROUND: Trigeminal ganglion (TG) plays an important role in the process of orthodontic pain. It's necessary to design an accurate, precise and minimally invasive trigeminal ganglion injection guide plate to study TG. METHODS: Micro-CT was used to obtain the Dicom format data, and three-dimensional (3D) software (mimics and magics23.03) was used to reconstruct 3D head models. Design and modifications of the TG injection guide plate were performed in Magic 23.03 software, and the guide plate was produced by a 3D stereolithography printer. X-ray, micro-CT, Evans blue, and virus transduction were used to demonstrate the accuracy of the guide-assisted injection. Pain levels were evaluated after using the injection guide by a bite force test and Von Frey test. RESULTS: X-ray and micro-CT tests confirmed that the injection needle reached the bilateral trigeminal ganglia fossa. The Evans blue test and virus transduction proved that the injected drug could be accurately injected into the bilateral trigeminal ganglion and the lentivirus could be successfully transfected. The percentage of accurate injection was 10/10 (bilateral trigeminal ganglia). Orofacial pain induced by the trigeminal ganglion injection was mild and returned to baseline within seven days. CONCLUSION: The injection guide described in this study is viable and reliable for the delivery of drugs and virus transduction into the trigeminal ganglia.

Does combining oro-facial manual therapy with bruxism neuroscience education affect pain and function in cases of awake bruxism? A pilot study.

BACKGROUND: Although awake bruxism is associated with temporomandibular disorder (TMD) as well as head and neck pain, the effects of physical therapy and bruxism education to address these factors have not been investigated. OBJECTIVE: The aim of this study was to evaluate the effects of oro-facial manual therapy and bruxism neuroscience education (BNE) on awake bruxism over a 3-week period with an open-ended follow-up questionnaire after 3 months. METHODS: Subjects (n = 28) were randomly allocated to one of two groups, an intervention group and a control group. Data regarding disability, function and pain were collected pre- and post-assessment, with all measures administered in a single-blind fashion. Participants in both groups received six treatment sessions during this period. In addition to manual therapy, participants were provided with information on the neurophysiological mechanisms of bruxism and contributing factors. Individual behavioural guidelines and daily exercises were determined in consultation with the therapist. An introduction to a bruxism specific app (Brux.App) was also provided, which all participants used as an adjunct to their treatment. RESULTS: The intervention group demonstrated notable improvement as indicated by their scores in the Neck Disability Index (NDI) (p = .008), Pain Disability Index (PDI) (p = .007) and Jaw Disability List (JDL) (p = .03). Furthermore, clinical assessments of the temporomandibular joint (TMJ) revealed a significant progress in terms of mouth opening (p = .03) and lateral jaw movement (laterotrusion) (p = .03). The mechanical pain threshold (PTT) of both the masseter (p = .02) and temporalis muscle (p = .05) also showed significant improvement. At 3-month follow-up, the questionnaire revealed that the majority of the intervention group (13/15, 87%) reported a benefit from the treatment. CONCLUSION: The reduction in pain and disability together with improvement in function and increased coping suggest a potential modification of awake bruxism through specialised musculoskeletal intervention and BNE tailored to the individual patient.