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Burning mouth syndrome (BMS) is a chronic pain condition lasting more than 3-6 months. While various pharmacological treatments are used, no definitive treatment exists. Autogenic training (AT), a relaxation technique, helps manage stress-related pain by influencing brain regions involved in emotion regulation and cognitive control. Reduced conditioned pain modulation (CPM) efficiency occurs in chronic pain conditions, and in BMS, higher state anxiety negatively impacts the descending pain modulation system. This study aimed to evaluate the effect of AT on spontaneous pain reduction in patients with BMS and determine if AT improves CPM, particularly in those with chronic BMS. This study included 28 patients diagnosed with BMS, along with 17 healthy volunteers. Based on the duration the patients experienced the pain, those with BMS were categorized into subchronic (≤6 months) and chronic (>6 months) groups. All participants' temporal summation of pain (TSP), CPM, and pain intensity were recorded before and after the AT intervention. TSP was assessed through repeated electrical stimulation to the chin and was calculated as the difference between the visual analog scale scores after 10 electrical stimuli and the score following the first stimulus. CPM was calculated as the difference in TSP at baseline and following the conditioning of painful (47°C) or non-painful (40°C) stimuli applied to the non-dominant hand, serving as the conditioning stimulus (CS). This study was approved by the Ethical Committee of the Nihon University School of Dentistry (EP21D002) and conducted in accordance with the Declaration of Helsinki. AT significantly reduced spontaneous pain in the chronic BMS group but not in the subchronic group. Furthermore, CPM improved only in patients with chronic BMS during painful stimuli, suggesting enhanced pain modulation. Correlation analysis between BMS duration and CPM revealed a negative correlation between painful CS CPM and disease duration (r = -0.411, p < 0.05), but no correlation when the CS was not painful. AT can reduce pain in patients with chronic BMS (lasting more than six months) at least partly by enhancing the patients' pain modulation and emotional regulation, making it a potential adjunctive therapy for chronic cases.

According to the International Classification of Headache Disorders, Third edition (ICHD-3), abdominal migraine is a diagnosis of exclusion, characterized by recurrent abdominal pain accompanied by nausea, vomiting, anorexia, or pallor. We report a case of a 44-year-old female with abdominal migraine associated with chronic apical periodontitis. Treatment with root canal therapy and periodontal management improved both the oral condition and migraine symptoms. Chronic periodontitis may contribute to migraines via systemic inflammation and calcitonin gene-related peptide (CGRP)-mediated neurovascular mechanisms. This case underscores the importance of dental practitioners identifying and managing periodontal conditions to address potential systemic effects and multifactorial orofacial pain.

Trigeminal nerve injury is known to cause severe persistent pain in the orofacial region. This pain is difficult to diagnose and treat. Recently, many animal studies have reported that rewiring of the peripheral and central nervous systems, non-neuronal cell activation, and up- and down-regulation of various molecules in non-neuronal cells are involved in the development of this pain following trigeminal nerve injury. However, there are many unknown mechanisms underlying the persistent orofacial pain associated with trigeminal nerve injury. In this review, we address recent animal data regarding the involvement of various molecules in the communication of neuronal and non-neuronal cells and examine the possible involvement of ascending pathways in processing pathological orofacial pain. We also address the clinical observations of persistent orofacial pain associated with trigeminal nerve injury and clinical approaches to their diagnosis and treatment.

Combined risk factors such as total gastrectomy, heavy alcohol consumption, smoking, and poor oral hygiene may contribute to the development of pulmonary actinomycosis. Here, we present a rare case of pulmonary actinomycosis triggered by total gastrectomy and heavy alcohol consumption. The patient presented with hemoptysis and a suspected lung mass. With a history of total gastrectomy and heavy alcohol consumption, the patient underwent imaging studies that initially suggested lung cancer. While imaging studies initially suggested lung cancer, multiple bronchoscopic examinations ultimately led to a diagnosis of pulmonary actinomycosis, following an initial biopsy that revealed chronic bronchitis. The patient was treated with oral amoxicillin (1,500 mg/day for six months) alongside comprehensive dental care, including periodontal therapy and dental restorations. This approach resulted in significant clinical improvement, with no recurrence of hemoptysis and favorable findings on chest X-ray. This case highlights the intricate interplay of risk factors in the development of pulmonary actinomycosis. It underscores the effectiveness of a multidisciplinary treatment strategy combining antibiotic therapy and dental care, which improved the patient's condition and avoided unnecessary interventions such as lung resection.

Background Chronic neuropathic pain, particularly in the orofacial region, markedly reduces quality of life. Peripheral trigeminal nerve injury activates satellite glial cells (SGCs) in the trigeminal ganglion (TG), which contributes to orofacial neuropathic pain. However, the upstream signal responsible for SGC activation remains unclear. This study investigated the role and cellular sources of interferon gamma (IFN-γ) signaling in the TG following infraorbital nerve injury (IONI) in rats. Methods Mechanical sensitivity of the whisker pad skin was assessed after IONI. Changes in IFN-γ levels, IFN-γ receptor expression, and glial fibrillary acidic protein (GFAP; a marker of SGC activation) were examined in the TG by immunohistochemistry. The effects of intra-TG administration of IFN-γ, an IFN-γ receptor antagonist, and isolated CD8⁺ T cells on mechanical hypersensitivity were evaluated. GFAP expression after intra-TG administration of IFN-γ or the receptor antagonist was also quantified. Flow cytometry and immunohistochemistry were used to identify IFN-γ–producing cells. In primary SGC cultures, IFN-γ–induced interleukin-1β (IL-1β) release was measured, and the impact of IL-1 receptor (IL-1R1) antagonism on mechanical hypersensitivity was tested. IL-1R1 localization and expression in TG neurons was further evaluated after IONI. Results IONI induced persistent mechanical hypersensitivity and upregulated IFN-γ, IFN-γ receptor, and GFAP expression in the TG. CD8⁺ T cells were the primary source of IFN-γ after IONI, and intra-TG transfer of isolated CD8⁺ T cells transiently induced mechanical hypersensitivity. IFN-γ receptors were localized to SGCs, with expression levels increasing after IONI. Intra-TG IFN-γ administration triggered mechanical hypersensitivity and SGC activation, and its receptor antagonism attenuated the hypersensitivity. IFN-γ stimulation of cultured SGCs enhanced IL-1β release. Co-administration of an IL-1R1 antagonist prevented IFN-γ–induced mechanical hypersensitivity. IL-1R1 was localized on TG neurons and were upregulated following IONI. Conclusions CD8⁺ T cell–derived IFN-γ activates SGCs in the TG, leading to IL-1β release that promotes neuronal hyperactivity and orofacial neuropathic pain following IONI. Targeting the IFN-γ–SGC–IL-1β signaling axis may represent a novel therapeutic strategy for orofacial neuropathic pain. Graphical Abstract

We evaluated the mechanisms underlying the oxytocin (OXT)-induced analgesic effect on orofacial neuropathic pain following infraorbital nerve injury (IONI). IONI was established through tight ligation of one-third of the infraorbital nerve thickness. Subsequently, the head withdrawal threshold for mechanical stimulation (MHWT) of the whisker pad skin was measured using a von Frey filament. Trigeminal ganglion (TG) neurons innervating the whisker pad skin were identified using a retrograde labeling technique. OXT receptor-immunoreactive (IR), transient receptor potential vanilloid 1 (TRPV1)-IR, and TRPV4-IR TG neurons innervating the whisker pad skin were examined on post-IONI day 5. The MHWT remarkably decreased from post-IONI day 1 onward. OXT application to the nerve-injured site attenuated the decrease in MHWT from day 5 onward. TRPV1 or TRPV4 antagonism significantly suppressed the decrement of MHWT following IONI. OXT receptors were expressed in the uninjured and Fluoro-Gold (FG)-labeled TG neurons. Furthermore, there was an increase in the number of FG-labeled TRPV1-IR and TRPV4-IR TG neurons, which was inhibited by administering OXT. This inhibition was suppressed by co-administration with an OXT receptor antagonist. These findings suggest that OXT application inhibits the increase in TRPV1-IR and TRPV4-IR TG neurons innervating the whisker pad skin, which attenuates post-IONI orofacial mechanical allodynia.

This passage discusses a case of trigeminal neuralgia (TN) with continuous pain and hemifacial spasm caused by vertebrobasilar dolichoectasia, a rare condition. The patient experienced ongoing orofacial pain, which initially led to dental treatments. After unsuccessful medication (carbamazepine), the patient underwent microvascular decompression to alleviate nerve compression by the elongated vertebral artery. This report highlights the challenge of treating such cases due to the unique nature of neurovascular compression. Additionally, it introduces the concept of TN with concomitant continuous pain and emphasizes the need for comprehensive diagnosis, as vertebrobasilar artery elongation is associated with various symptoms, including TN and hemifacial spasms.

Orofacial pain conditions are complex disorders that involve biological, social, and psychological factors. Temporomandibular Disorders (TMDs) are one of the most common orofacial pain conditions, and our previous literature review indicated that exercise therapy has shown promise in reducing TMD-related pain. However, more evidence is needed to firmly establish its effectiveness. This systematic review aims to investigate the effectiveness of exercise therapy on pain relief and jaw mobility in patients with pain-related TMDs. To include randomized controlled trials (RCTs) written in English, a literature search was performed using PubMed, Scopus, Web of Science, Cochrane Library, Ovid, EBM reviews, and Academic Search Complete initially from 4th November 2020 until March 2022. A PICOS for this review was as follows; P: Patients with TMD myalgia or arthralgia, I: Excursion exercise, Stretch exercises, Resistance exercise, or Coordination exercise, C: No treatment or education only. O: Pain intensity and Range of Motion (ROM), S: RCTs. After title screening, a full-text assessment was done to extract data. According to Risk of Bias (RoB) 2.0, risk of bias was assessed in each included paper by 2 reviewers independently. A total of 3,388 titles were identified from the electronic database search. After the screening and full-text evaluation, only 5 studies (145 participants) were eligible to be included. Among the exercise modalities, coordination exercise showed a significant effect on pain relief and improvement of joint mobility. Due to the heterogeneity and small sample size of the included studies, a meta-analysis was not feasible. However, this systematic review suggested that exercise therapy, especially coordinate exercise, can be effective in managing painful TMD conditions. Further research is needed to establish optimal parameters for this patient population, as well as standardization and consistency in terminology and treatment structure.

Calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia (CREST) syndrome, a systemic sclerosis subtype, features skin thickening, vascular issues, and organ involvement, causing complications in the gastrointestinal and musculoskeletal systems. Herein, we present a rare case of oral candidiasis, with CREST syndrome. The patient presented with xerostomia, tongue erythema, and burning pain. The patient reported finger stiffness, facial sclerosis, cold-induced pain, and a 10-year history of palmar-plantar pustulosis. Laboratory tests confirmed antinuclear antibodies (ANA) and anticentromere antibodies (1:1280), leading to a diagnosis of CREST syndrome. A fungal culture identified , and treatment with miconazole gel successfully resolved the infection. This case emphasizes the importance of recognizing oral manifestations in systemic autoimmune diseases, as conditions like xerostomia increase susceptibility to infections.