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The prevalence of temporomandibular disorder (TMD) among elderly people with Parkinson's disease (PD) is relatively high, but a population-based study of the relationship between PD and TMD is still lacking. This study, therefore, sought to investigate the association between TMD and PD by using data for one million randomly sampled beneficiaries of Taiwan's National Health Insurance program, including 6,185 PD patients who were matched through propensity score matching with 18,555 non-PD patients. Both the PD and non-PD cohorts were followed until death, any diagnosis of TMD, or December 31, 2013, whichever occurred first. Each diagnosis of TMD was made by a qualified physician according to the International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM), using the diagnosis codes 524.60, 524.62, 524.63, and 524.69 while excluding tooth abscess, wisdom tooth eruption, herpes zoster and postherpetic neuralgia, mastoiditis, otitis externa, otitis media, parotitis, sialadenitis, and trigeminal neuralgia. We used Cox proportional hazard regression models to calculate the relative risk of TMD and found a 2.11-fold (95% CI: 1.35-3.30) increased risk of TMD overall in the PD group compared with the non-PD group. Stratified by follow-up period, there was a 4.25-fold (95% CI: 1.51-11.93) increased risk in the PD group in the first year after the initial PD diagnosis and a 3.88-fold (95% CI: 1.33-11.28) increased risk in the second year. Over the long-term (>5 years), PD was significantly associated with an increased risk of TMD. These findings suggest that it is important to closely monitor the temporomandibular joint health of PD patients.

The deficiency of clinically specific biomarkers has made it difficult to achieve an accurate diagnosis of temporomandibular joint osteoarthritis (TMJ-OA) and the insufficient comprehension of the pathogenesis of the pathogenesis of TMJ-OA has posed challenges in advancing therapeutic measures. The combined use of metabolomics and transcriptomics technologies presents a highly effective method for identifying vital metabolic pathways and key genes in TMJ-OA patients. In this study, an analysis of synovial fluid untargeted metabolomics of 6 TMJ-OA groups and 6 temporomandibular joint reducible anterior disc displacement (TMJ-DD) groups was conducted using liquid and gas chromatography mass spectrometry (LC/GC-MS). The differential metabolites (DMs) between TMJ-OA and TMJ-DD groups were analyzed through multivariate analysis. Meanwhile, a transcriptomic dataset (GSE205389) was obtained from the GEO database to analyze the differential metabolism-related genes (DE-MTGs) between TMJ-OA and TMJ-DD groups. Finally, an integrated analysis of DMs and DE-MTGs was carried out to investigate the molecular mechanisms associated with TMJ-OA. The analysis revealed significant differences in the levels of 46 DMs between TMJ-OA and TMJ-DD groups, of which 3 metabolites (L-carnitine, taurine, and adenosine) were identified as potential biomarkers for TMJ-OA. Collectively, differential expression analysis identified 20 DE-MTGs. Furthermore, the integration of metabolomics and transcriptomics analysis revealed that the tricarboxylic acid (TCA) cycle, alanine, aspartate and glutamate metabolism, ferroptosis were significantly enriched. This study provides valuable insights into the metabolic abnormalities and associated pathogenic mechanisms, improving our understanding of TMJOA etiopathogenesis and facilitating potential target screening for therapeutic intervention.

The temporomandibular joint (TMJ) is a fibrocartilaginous tissue critical for chewing and speaking. In patients with temporomandibular disorders (TMDs), permanent tissue loss can occur. Recapitulating the complexity of TMDs in animal models is difficult, yet critical for the advent of new therapies. Synovial fluid from diseased human samples revealed elevated levels of tumor necrosis factor alpha (TNF-alpha). Here, we propose to recapitulate these findings in mice by subjecting murine TMJs with TNF-alpha or CFA (Complete Freund's Adjuvant) in mandibular condyle explant cultures and by local delivery in vivo using TMJ intra-articular injections. Both TNF-alpha and CFA delivery to whole mandibular explants and in vivo increased extracellular matrix deposition and increased cartilage thickness, while TNF-alpha treated explants had increased expression of inflammatory cytokines and degradative enzymes. Moreover, the application of TNF-alpha or CFA in both models reduced cell number. CFA delivery in vivo caused soft tissue inflammation, including pannus formation. Our work provides two methods of chemically induced TMJ inflammatory arthritis through a condyle explant model and intra-articular injection model that replicate findings seen in synovial fluid of human patients, which can be used for further studies delineating the mechanisms underlying TMJ pathology.

Craniofacial asymmetry, mandibular condylar modeling and temporomandibular joint disorders are common comorbidities of skeletally disproportionate malocclusions, but etiology of occurrence together is poorly understood. We compared asymmetry, condyle modeling stability and temporomandibular health in a cohort of 128 patients having orthodontics and orthognathic surgery to correct dentofacial deformity malocclusions. We also compared ACTN3 and ENPP1 genotypes for association to clinical conditions. Pre-surgical posterior-anterior cephalometric and panometric radiographic analyses; jaw pain and function questionnaire and clinical examination of TMD; and SNP-genotype analysis from saliva samples were compared to assess interrelationships. Almost half had asymmetries in need of surgical correction, which could be subdivided into four distinct morphological patterns. Asymmetric condyle modeling between sides was significantly greater in craniofacial asymmetry, but most commonly had an unanticipated pattern. Often, longer or larger condyles occurred on the shorter mandibular ramus side. Subjects with longer ramus but dimensionally smaller condyles were more likely to have self-reported TMD symptoms (p = 0.023) and significantly greater clinical diagnosis of TMD (p = 0 .000001), with masticatory myalgia most prominent. Genotyping found two significant genotype associations for ACTN3 rs1671064 (Q523R missense) p = 0.02; rs678397 (intronic SNP) p = 0.04 and one significant allele association rs1815739 (R577X nonsense) p = 0.00. Skeletal asymmetry, unusual condyle modeling and TMD are common and interrelated components of many dentofacial deformities. Imbalanced musculoskeletal functional adaptations and genetic or epigenetic influences contribute to the etiology, and require further investigation.

To explore the role of YAP, a key effector of the Hippo pathway, in temporomandibular joint (TMJ) ankylosis. The temporal and spatial expression of YAP was detected via immunohistochemistry and multiplex immunohistochemistry on postoperative Days 1, 4, 7, 9, 11, 14 and 28 in a sheep model. Isolated mesenchymal stem cells (MSCs) from samples of the Day 14. The relative mRNA expression of YAP was examined before and after the osteogenic induction of MSCs. A YAP-silenced MSC model was constructed, and the effect of YAP knockdown on MSC function was examined. YAP is expressed in the nucleus of the key sites that determine the ankylosis formation, indicating that YAP is activated in a physiological state. The expression of YAP increased gradually over time. Moreover, the number of cells coexpressing of RUNX2 and YAP—with the osteogenic active zone labelled by RUNX2—tended to increase after Day 9. After the osteogenic induction of MSCs, the expression of YAP increased. After silencing YAP, the osteogenic, proliferative and migratory abilities of the MSCs were inhibited. YAP is involved in the early development of TMJ bony ankylosis. Inhibition of YAP using shRNA might be a promising way to prevent or treat TMJ ankylosis.

While numerous studies have underscored the implication of immune cells and metabolites in temporomandibular disorders (TMD), conclusive evidence for causality remains elusive. Consequently, our aim is to explore the causal connections between immunophenotypes and plasma metabolites in relation to TMD employing a bidirectional Mendelian randomization (MR) approach. Summary statistics data on 731 immunophenotypes (n = 3757) and 1091 plasma metabolites (n = 8299) were obtained from comprehensive genome-wide association studies (GWAS), while TMD data (5668 cases and 205,355 controls) were acquired from the FinnGen Consortium. Bidirectional MR analyses and a two-step MR approach assessed causal relationships and potential intermediaries. Various corrections and sensitivity analyses were utilized to assess the robustness of the findings. Two immunophenotypes and seven metabolites were significantly associated with TMD risk. Specifically, Alpha-hydroxyisovalerate mediated the link between CD33 on CD33dim HLA DR + CD11b + and TMD (β = 0.034, P  = 5.95 × 10 –5 ), while CD8 on NKT cells mediated the causal relationship between 5-acetylamino-6-formylamino-3-methyluracil levels and TMD (β = 0.069, P  = 5.11 × 10 –5 ). Our findings revealed the causal relationships between immunophenotypes and plasma metabolites on TMD from a genetic perspective, potentially aiding in TMD prevention.

This case-control study aimed to investigate variables based on a cognitive-behavioral-emotional model related to the development of painful temporomandibular disorders (TMD) in a sample of monozygotic twins discordant for the condition. This case-control study investigated 20 monozygotic twins (10 pairs discordant for painful TMD), aged between 18 and 55. Participants were recruited through a comprehensive strategy following ethical approval, with inclusion criteria disseminated via social media, websites, local radio, messaging apps, and physical posters in public and healthcare spaces in Ribeirão Preto.The diagnosis of painful TMD was determined according to the Diagnostic Criteria for Temporomandibular Disorders - Brazilian Portuguese (DC/TMD). The cognitive-behavioral-emotional variables analyzed were a sociodemographic profile, pain sensitivity (pain threshold to pressure, allodynia, and hyperalgesia), oral behaviors, pain vigilance and awareness, pain catastrophizing, central sensitization, stress, anxiety, depression, alexithymia, mindfulness facets, sleep quality, pain control, pain intensity and interference, trigeminal and extra trigeminal pain areas. Bivariate logistic regression models were used to identify factors associated with TMD (p < 0.20), followed by multicollinearity analysis using Spearman's correlation to exclude highly correlated variables. The final multiple logistic regression model included independent predictors to ensure robustness and accurate estimates, with statistical significance set at α = 0.05. While the adjusted model did not identify statistically significant associations, variables such as increased pain sensitivity in the masseter muscle (OR = 3.29, 95% CI: 0.17-62.8, p = 0.428), higher levels of pain catastrophizing (OR = 1.08, 95% CI: 0.64-1.8, p = 0.776), difficulty in externalizing feelings (OR = 1.61, 95% CI: 0.13-2.9, p = 0.539), and higher scores on the distraction facet of mindfulness (OR = 4.65, 95% CI: 0.39-55.7, p = 0.225) were included due to their clinical relevance and their significant associations in the bivariate analysis (p < 0.20). Our study highlights the potential clinical relevance of cognitive-behavioral-emotional variables, such as increased pain sensitivity in the masseter muscle, higher levels of pain catastrophizing, difficulty in externalizing feelings, and higher scores on the distraction facet of mindfulness, in understanding painful TMD. While these variables did not show statistical significance in the adjusted model, their inclusion underscores the importance of exploring these factors in clinical practice. Further research is needed to validate these findings and clarify their role in the development and management of painful TMD. This study underscores the importance of cognitive-behavioral-emotional factors in the context of painful TMD, suggesting that variables like pain sensitivity and emotional regulation may be valuable for clinical assessment and management strategies. Despite the lack of statistically significant associations, these findings provide a foundation for future research to better understand and address the multidimensional nature of TMD in clinical practice.

Background Resistance to treatments have been assessed in chronic conditions such as migraine, but not in temporomandibular disorders (TMD). This study aimed to identify factors that influence treatment outcome in patients with myofascial TMD pain. Methods Seventy-two females were divided into three groups: TMD successfully treated (TMD-S, n  = 24), TMD resistant to treatment (TMD-R, n  = 24) and Controls without TMD ( n  = 24). Criteria for resistance included: less than 30% pain reduction after three months of conservative treatment and an average pain intensity > 50 mm (VAS) during the last month. Quantitative sensory testing (QST), psychosocial status and genetic polymorphisms were examined. ANOVA on ranks (psychosocial variables) with Dunn’s test as post-hoc or ANOVA (age and somatosensory variables) with Tukey test as post-hoc test, and Dwass-Steel-Critchlow-Fligner test (genetic variables) were used for univariate groups comparisons. Multivariate statistics were used to identify outcomes that separated the groups. Results QST assessment revealed lower baseline pressure pain threshold and higher wind-up ratio in the trigeminally and spinally innervated areas in the TMD-R group compared with the other groups ( p  = 0.01). Also, the TMD-R group presented higher values in all assessed psychosocial variables ( p  < 0.01) and higher prevalence of the HTR1A polymorphism rs6295 ( p  = 0.02) compared with the other groups at baseline. Multivariate analysis showed that the three variables that distinguished the best between TMD-R and TMD-S were sleeping quality, central sensitization, and depressive symptoms. Conclusion Psychosocial, somatosensory, and genetic alterations are related to unsuccessful treatment response in myofascial TMD patients.

The role of autoimmune diseases (ADs) in temporomandibular disorders (TMDs) has been emphasized in observational studies. However, whether the causation exists is unclear, and controversy remains about which specific disorder is destructive in TMDs. This Mendelian randomization (MR) study aims to estimate the causal effect of common ADs on TMDs. Genetic data from published genome-wide association studies for fourteen common ADs, specifically multiple sclerosis (MS, N = 15,283), ankylosing spondylitis (AS, N = 22,647), asthma (N = 408,422), celiac disease (N = 15,283), Graves' disease (N = 458,620), Hashimoto thyroiditis (N = 395,640), primary biliary cirrhosis (PBC, N = 11,375), primary sclerosing cholangitis (PSC, N = 14,890), psoriasis vulgaris (N = 483,174), rheumatoid arthritis (RA, N = 417,256), systemic lupus erythematosus (SLE, N = 23,210), Type 1 diabetes (T1D, N = 520,580), inflammatory bowel disease (IBD, N = 34,652), and Sjogren's syndrome (SS, N = 407,746) were collected. Additionally, the latest summary-level data for TMDs (N = 228,812) were extracted from the FinnGen database. The overall effects of each immune traits were assessed via inverse-variance weighted (IVW), weighted median, and MR-Egger methods, and performed extensive sensitivity analyses. Finally, 731 immune cell phenotypes (N = 3,757) were analyzed for their mediating role in the significant causality. Univariable MR analyses revealed that genetically predicted RA (IVW OR: 1.12, 95% CI: 1.05-1.19, < 0.001) and MS (IVW OR: 1.06, 95% CI: 1.03-1.10, = 0.001) were associated with increased risk of TMDs. Two out of 731 immune cell phenotypes were identified as causal mediators in the associations of RA with TMDs, including \"CD25++ CD8+ T cell % CD8+ T cell\" (mediation proportion: 6.2%) and \"CD3 on activated CD4 regulatory T cell\" (5.4%). Additionally, \"CD127 on granulocyte\" mediated 10.6% of the total effect of MS on TMDs. No reverse directions, heterogeneity, and pleiotropy were detected in the analyses ( > 0.05). This MR study provides new evidence regarding the causal impact of genetic predisposition to RA or MS on the increased risk of TMDs, potentially mediated by the modulation of immune cells. These findings highlight the importance for clinicians to pay more attention to patients with RA or MS when consulting for temporomandibular discomfort. The mediating role of specific immune cells is proposed but needs further investigation.

Osteoarthritis (OA) of the temporomandibular joint (TMJ) is a progressive disease characterized by the progressive destruction of the internal surfaces of the joint. Certain epigenetic biomarkers have been detected in TMJ-OA. We summarized the available evidence on the epigenetic biomarkers in TMJ-OA. There is an increase in the expression of non-coding RNAs related to the degradation of the extracellular matrix, chondrocyte apoptosis, and proinflammatory cytokines, while there is a decrease in the expression of those related to COL2A1, as well as the osteogenic and chondrogenic differentiation of mesenchymal stem cells. Certain methylated genes and histone modifications in TMJ-OA were also identified. In the early stage, DNA methylation was significantly decreased; that is, the expression of inflammation-related genes such as TNF and genes associated with extracellular matrix degradation, such as Adamts, were increased. While in the late stage, there was an increase in the expression of genes associated with the TGF-β and MAPK signaling pathway and angiogenesis-related genes. Although research on the role of epigenetic markers in TMJ-OA is still ongoing, the results here contribute to improving the basis for the identification of accurate diagnostic and prognostic markers and the development of new therapeutic molecules for the prevention and management of TMJ-OA. It also represents a significant advancement in elucidating its pathogenesis.