Temporomandibular disorders.
Ontology highlight
ABSTRACT:
SUBMITTER: Palmer J
PROVIDER: S-EPMC7810821 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The temporomandibular joint (TMJ) has many essential functions. None of its components are exempt from injury. Facial asymmetry, malocclusion, disturbances in growth, osteoarthritis, and ankylosis can manifest as complications from trauma to the TMJ. The goals of initial treatment include achievement of pretraumatic function, restoration of facial symmetry, and resolution of pain. These same objectives hold true for late repairs and reconstruction of the TMJ apparatus. Treatment is demanding, and with opposing approaches. The following article explores various treatment options for problems presenting as a result of a history of trauma to the TMJ.
| S-EPMC3052671 | biostudies-other
Project description:By analogy with the journal's title Pain Research and Management, this review describes TMD Research and Management. More specific are the (1) research aspects of "occlusion," still one of the most controversial topics in TMD, and (2) as much as possible evidence-based management aspects of "TMD" for the dental practitioner. Research. The disorders temporomandibular dysfunction and the synonymous craniomandibular dysfunction are still being discussed intensely in the literature. Traditionally, attention is mostly devoted to occlusion and its relationship with these disorders. The conclusions reached are often contradictory. Considering the definitions of temporomandibular and craniomandibular dysfunctions/disorders and "occlusion," a possible explanation for this controversy can be found in the subsequent methodological problems of the studies. Based on a Medline search of these terms over the past 40 years related to contemporary terms such as "Evidence Based Dentistry" and "Pyramid of Evidence," these methodological aspects are examined, resulting in recommendations for future research and TMD-occlusal therapy. Management. To assist the dental practitioner in his/her daily routine to meet the modern standards of best practice, 7 guidelines are formulated that are explained and accompanied with clinical examples for an evidence-based treatment of patients with this disorder in general dental practices.
| S-EPMC5976904 | biostudies-literature
Project description:Multiple physiological and psychological regulatory domains may contribute to the pathophysiology of pain in temporomandibular disorder (TMD) and other bodily pain conditions. The purpose of this study was to evaluate the relationship between multisystem dysregulation and the presence of TMD pain, as well as the presence of different numbers of comorbid pain conditions in TMD. Secondary data analysis was conducted in 131 non-TMD (without comorbid pain) controls, 14 TMD subjects without comorbid pain, 78 TMD subjects with 1 comorbid pain, and 67 TMD subjects with multiple comorbid pain conditions who participated in a TMD genetic study. Twenty markers from sensory, autonomic, inflammatory, and psychological domains were evaluated. The results revealed that 1) overall dysregulation in multiple system domains (OR [odds ratio] = 1.6, 95% confidence interval [CI] = 1.4-1.8), particularly in the sensory (OR = 1.9, 95% CI = 1.3-2.9) and the psychological (OR = 2.1, 95% CI = 2.1-2.7) domains, were associated with increased likelihood of being a painful TMD case; and 2) dysregulations in individual system domains were selectively associated with the increased odds of being a TMD case with different levels of comorbid persistent pain conditions. These outcomes indicate that heterogeneous multisystem dysregulations may exist in painful TMD subgroups, and multidimensional physiological and psychological assessments can provide important information regarding pathophysiology, diagnosis, and management of pain in TMD patients.The concurrent assessment of multiple physiological and psychological systems is critical to our understanding of the pathophysiological processes that contribute to painful TMD and associated comorbid conditions, which will ultimately guide and inform appropriate treatment strategies that address the multisystem dysregulation associated with complex and common persistent pain conditions.
| S-EPMC3770463 | biostudies-literature
Project description: Not available
| S-EPMC9370076 | biostudies-literature
Project description:The aim of this study was to identify correlations between sleep bruxism (SB) and temporomandibular disorders (TMD) as diagnosed by means of the research diagnostic criteria for temporomandibular disorders (RDC/TMD). Sleep bruxism was diagnosed on the basis of I) validated questionnaires, II) clinical symptoms, and III) electromyographic/electrocardiographic data. A total of 110 subjects were included in the study. Fifty-eight patients were identified as bruxers and 52 as nonbruxers. A psychosocial assessment was also performed. An RDC/TMD group-I diagnosis (myofascial pain) was made for 10 out of 58 bruxers, whereas none of the nonbruxers received a diagnosis of this type. No significant differences were found between bruxers and nonbruxers with regard to RDC/TMD group-II (disc displacement) and group-III (arthralgia, arthritis, arthrosis) diagnoses. Somatization was significantly more common among bruxers than nonbruxers. Multivariate logistic regression analysis revealed that somatization was the only factor significantly correlated with the diagnosis of myofascial pain. The results of this study indicate a correlation between myofascial pain, as diagnosed using the RDC/TMD, and somatization. It seems that somatization is a stronger predictor of an RDC/TMD diagnosis of myofascial pain than sleep bruxism is.
| S-EPMC7074179 | biostudies-literature
Project description:The aims of this study were (1) to compare the levels and interactions of several plasma proteins in patients with myogenous temporomandibular disorders (TMDM) compared to healthy and pain-free controls, (2) to compare the levels and interactions in two TMDM subgroups, myalgia (MYA) and myofascial pain (MFP), and (3) to explore associations between the proteins and clinical data. Thirty-nine patients with TMDM (MFP, n = 25, MYA, n = 14), diagnosed according to the diagnostic criteria for TMD (DC/TMD), aged 38 years, and sex-matched pain-free controls completed an extended DC/TMD Axis II questionnaire and the plasma concentration of 87 biomarkers were analyzed. Nine proteins separated TMDM from controls (p = 0.0174) and 12 proteins separated MYA from MFP (p = 0.019). Pain duration, characteristic pain intensity, pain catastrophizing, perceived stress, and insomnia severity were significantly associated with protein markers (p < 0.001 to p < 0.022). In conclusion, several plasma proteins were upregulated in TMDM and either upregulated or downregulated in MYA compared to MFP. Some proteins in TMDM were associated with pain variables, sleep disturbance, and emotional function. These results show that systemic differences in protein expression exist in patients with TMDM and that altered levels of specific plasma proteins are associated with different clinical variables.
| S-EPMC9144449 | biostudies-literature
Project description:Although temporomandibular disorders (TMD) have been associated with abnormal gray matter volumes in cortical areas and in the striatum, the corticostriatal functional connectivity (FC) of patients with TMD has not been studied. Here, we studied 30 patients with TMD and 20 healthy controls that underwent clinical evaluations, including Helkimo indices, pain assessments, and resting-state functional magnetic resonance imaging scans. The FCs of the striatal regions with the other brain areas were examined with a seed-based approach. As seeds, we used the dorsal caudate, ventral caudate/nucleus accumbens, dorsal caudal putamen, and ventral rostral putamen regions. Voxel-wise comparisons with controls revealed that the patients with TMD exhibited reduced FCs in the ventral corticostriatal circuitry, between the ventral striatum and ventral frontal cortices, including the anterior cingulate cortex and anterior insula; in the dorsal corticostriatal circuitry, between the dorsal striatum and the dorsal cortices, including the precentral gyrus and supramarginal gyrus; and also within the striatum. Additionally, we explored correlations between the reduced corticostriatal FCs and clinical measurements. These results directly supported the hypothesis that TMD is associated with reduced FCs in brain corticostriatal networks and that these reduced FCs may underlie the deficits in motor control, pain processing, and cognition in TMD. Our findings may contribute to the understanding of the etiologies and pathologies of TMD.
| S-EPMC6866295 | biostudies-literature
Project description:BackgroundPeriodontitis (PD) may affect temporomandibular joint disorders (TMD) and TMD may influence PD in previous observational studies. Nevertheless, these studies were prone to confounders and reverse causation, leading to incorrect conclusions about causality and direction of association. This research investigates the associations between PD and TMD employing bidirectional two-sample Mendelian randomization (MR) analysis.MethodsSingle-nucleotide polymorphisms (SNPs) related to PD (p < 5 × 10-6) were selected from a genome-wide association study (GWAS) from the Gene-Lifestyle Interaction in the Dental Endpoints (GLIDE) consortium, and related these to SNPs from FinnGen and UK Biobank (UKB) consortia, and vice versa. We implemented the standard inverse variance weighted (IVW), weighted median (WM), MR-Egger regression, and MR-PRESSO methods to estimate the potential causality between PD and TMD. Sensitive tests were conducted using robust MR methods. Results from FinnGen and UKB were combined using the fixed model.ResultsPD did not appear to causally affect TMD. Additionally, the reverse MR analysis did not reveal a significant causal effect of TMD on PD. The results of other MR methods were similar to those of the IVW method. Sensitivity analyses addressed no potential pleiotropy in MR estimations. Results from the meta-analysis were consistent with the above-mentioned consequences.ConclusionThis research does not support a causal relationship between PD and TMD. PD does not appear to worsen TMD directly, and vice versa.
| S-EPMC10408055 | biostudies-literature
Project description:In the last years, several attempts have been made to study specific biological markers of temporomandibular disorders (TMD). So far, no laboratory tests have been appropriately validated for the diagnosis and prognosis of these disorders. This study aimed to investigate the proteomic profile of the whole stimulated saliva of TMD myalgia patients in order to evaluate potential diagnostic and/or prognostic salivary candidate proteins which could be useful for the management of TMD. Twenty patients diagnosed with TMD myalgia according to the validated Diagnostic Criteria for TMD (DC/TMD) and 20 matched healthy pain-free controls were enrolled. Saliva samples were collected in the morning. Comparative proteomic analysis was performed with two-dimensional gel electrophoresis followed by identification with liquid chromatography-tandem mass spectrometry. Statistical analysis of the quantitative proteomics data revealed that 20 proteins were significantly altered in patients compared to controls. Among these proteins, 12 showed significantly increased levels, and 8 showed significantly decreased levels in patients with TMD myalgia compared to controls. The identified proteins are involved in metabolic processes, immune response, and stress response. This proteomic study shows that the salivary protein profile can discriminate patients with TMD myalgia from healthy subjects, but the protein signature has no correlation with the clinical features of TMD myalgia. Additional studies are needed to validate our observations in additional sample sets and to continue assessing the utility of saliva as a suitable sample for studying processes related to TMD myalgia.
| S-EPMC7177369 | biostudies-literature
Project description:Until recently, most clinicians and scientists believed that the experience of pain is perceptually proportional to the amount of incoming peripheral nociceptive drive due to injury or inflammation in the area perceived to be painful. However, many cases of chronic pain have defied this logic, leaving clinicians perplexed as to how patients are experiencing pain with no obvious signs of injury in the periphery. Conversely, there are patients who have a peripheral injury and/or inflammation but little or no pain. What makes some individuals experience intense pain with minimal peripheral nociceptive stimulation and others experience minimal pain with serious injury? It is increasingly well accepted in the scientific community that pain can be generated and maintained or, through other mechanisms, suppressed by changes in the central nervous system, creating a complete mismatch between peripheral nociceptive drive and perceived pain. In fact, there is no known chronic pain condition where the observed extent of peripheral damage reproducibly engenders the same level of pain across individuals. Temporomandibular disorders (TMDs) are no exception. This review focuses on the idea that TMD patients range on a continuum-from those whose pain is generated peripherally to those whose pain is centralized (i.e., generated, exacerbated, and/or maintained by central nervous system mechanisms). This article uses other centralized chronic pain conditions as a guide, and it suggests that the mechanistic variability in TMD pain etiology has prevented us from adequately treating many individuals who are diagnosed with the condition. As the field moves forward, it will be imperative to understand each person's pain from its own mechanistic standpoint, which will enable clinicians to deliver personalized medicine to TMD patients and eventually provide relief in even the most recalcitrant cases.
| S-EPMC5004242 | biostudies-literature