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      MRI-Based Assessment of Masticatory Muscle Changes in TMD Patients after Whiplash Injury

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          Abstract

          Objective: to investigate the change in volume and signal in the masticatory muscles and temporomandibular joint (TMJ) of patients with temporomandibular disorder (TMD) after whiplash injury, based on magnetic resonance imaging (MRI), and to correlate them with other clinical parameters. Methods: ninety patients (64 women, 26 men; mean age: 39.36 ± 15.40 years), including 45 patients with symptoms of TMD after whiplash injury (wTMD), and 45 age- and sex-matched controls with TMD due to idiopathic causes (iTMD) were included. TMD was diagnosed using the study diagnostic criteria for TMD Axis I, and MRI findings of the TMJ and masticatory muscles were investigated. To evaluate the severity of TMD pain and muscle tenderness, we used a visual analog scale (VAS), palpation index (PI), and neck PI. Results: TMD indexes, including VAS, PI, and neck PI were significantly higher in the wTMD group. In the wTMD group, muscle tenderness was highest in the masseter muscle (71.1%), and muscle tenderness in the temporalis (60.0%), lateral pterygoid muscle (LPM) (22.2%), and medial pterygoid muscle (15.6%) was significantly more frequent than that in the iTMD group (all p < 0.05). The most noticeable structural changes in the masticatory muscles occurred in the LPM with whiplash injury. Volume (57.8% vs. 17.8%) and signal changes (42.2% vs. 15.6%) of LPM were significantly more frequent in the wTMD group than in the iTMD group. The presence of signal changes in the LPM was positively correlated with the increased VAS scores only in the wTMD group (r = 0.346, p = 0.020). The prevalence of anterior disc displacement without reduction (ADDWoR) (53.3% vs. 28.9%) and disc deformity (57.8% vs. 40.0%) were significantly higher in the wTMD group ( p < 0.05). The presence of headache, sleep problems, and psychological distress was significantly higher in the wTMD group than in the iTMD group. Conclusion: abnormal MRI findings and their correlations with clinical characteristics of the wTMD group were different from those of the iTMD group. The underlying pathophysiology may differ depending on the cause of TMD, raising the need for a treatment strategy accordingly.

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          Diagnostic Criteria for Temporomandibular Disorders (DC/TMD) for Clinical and Research Applications: recommendations of the International RDC/TMD Consortium Network* and Orofacial Pain Special Interest Group†.

          The original Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD) Axis I diagnostic algorithms have been demonstrated to be reliable. However, the Validation Project determined that the RDC/TMD Axis I validity was below the target sensitivity of ≥ 0.70 and specificity of ≥ 0.95. Consequently, these empirical results supported the development of revised RDC/TMD Axis I diagnostic algorithms that were subsequently demonstrated to be valid for the most common pain-related TMD and for one temporomandibular joint (TMJ) intra-articular disorder. The original RDC/TMD Axis II instruments were shown to be both reliable and valid. Working from these findings and revisions, two international consensus workshops were convened, from which recommendations were obtained for the finalization of new Axis I diagnostic algorithms and new Axis II instruments. Through a series of workshops and symposia, a panel of clinical and basic science pain experts modified the revised RDC/TMD Axis I algorithms by using comprehensive searches of published TMD diagnostic literature followed by review and consensus via a formal structured process. The panel's recommendations for further revision of the Axis I diagnostic algorithms were assessed for validity by using the Validation Project's data set, and for reliability by using newly collected data from the ongoing TMJ Impact Project-the follow-up study to the Validation Project. New Axis II instruments were identified through a comprehensive search of the literature providing valid instruments that, relative to the RDC/TMD, are shorter in length, are available in the public domain, and currently are being used in medical settings. The newly recommended Diagnostic Criteria for TMD (DC/TMD) Axis I protocol includes both a valid screener for detecting any pain-related TMD as well as valid diagnostic criteria for differentiating the most common pain-related TMD (sensitivity ≥ 0.86, specificity ≥ 0.98) and for one intra-articular disorder (sensitivity of 0.80 and specificity of 0.97). Diagnostic criteria for other common intra-articular disorders lack adequate validity for clinical diagnoses but can be used for screening purposes. Inter-examiner reliability for the clinical assessment associated with the validated DC/TMD criteria for pain-related TMD is excellent (kappa ≥ 0.85). Finally, a comprehensive classification system that includes both the common and less common TMD is also presented. The Axis II protocol retains selected original RDC/TMD screening instruments augmented with new instruments to assess jaw function as well as behavioral and additional psychosocial factors. The Axis II protocol is divided into screening and comprehensive self report instrument sets. The screening instruments' 41 questions assess pain intensity, pain-related disability, psychological distress, jaw functional limitations, and parafunctional behaviors, and a pain drawing is used to assess locations of pain. The comprehensive instruments, composed of 81 questions, assess in further detail jaw functional limitations and psychological distress as well as additional constructs of anxiety and presence of comorbid pain conditions. The recommended evidence-based new DC/TMD protocol is appropriate for use in both clinical and research settings. More comprehensive instruments augment short and simple screening instruments for Axis I and Axis II. These validated instruments allow for identification of patients with a range of simple to complex TMD presentations.
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            The neuropathology of traumatic brain injury.

            Traumatic brain injury, a leading cause of mortality and morbidity, is divided into three grades of severity: mild, moderate, and severe, based on the Glasgow Coma Scale, the loss of consciousness, and the development of post-traumatic amnesia. Although mild traumatic brain injury, including concussion and subconcussion, is by far the most common, it is also the most difficult to diagnose and the least well understood. Proper recognition, management, and treatment of acute concussion and mild traumatic brain injury are the fundamentals of an emerging clinical discipline. It is also becoming increasingly clear that some mild traumatic brain injuries have persistent, and sometimes progressive, long-term debilitating effects. Evidence indicates that a single traumatic brain injury can precipitate or accelerate multiple age-related neurodegenerations, increase the risk of developing Alzheimer's disease, Parkinson's disease, and motor neuron disease, and that repetitive mild traumatic brain injuries can provoke the development of a tauopathy, chronic traumatic encephalopathy. Clinically, chronic traumatic encephalopathy is associated with behavioral changes, executive dysfunction, memory loss, and cognitive impairments that begin insidiously and progress slowly over decades. Pathologically, chronic traumatic encephalopathy produces atrophy of the frontal and temporal lobes, thalamus, and hypothalamus, septal abnormalities, and abnormal deposits of hyperphosphorylated tau (τ) as neurofibrillary tangles and disordered neurites throughout the brain. The incidence and prevalence of chronic traumatic encephalopathy and the genetic risk factors critical to its development are currently unknown. Chronic traumatic encephalopathy frequently occurs as a sole diagnosis, but may be associated with other neurodegenerative disorders, including Alzheimer's disease, Lewy body disease, and motor neuron disease. Currently, chronic traumatic encephalopathy can be diagnosed only at autopsy; however, promising efforts to develop imaging, spinal fluid, and peripheral blood biomarkers are underway to diagnose and monitor the course of disease in living subjects.
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              Fatty Infiltration of Skeletal Muscle: Mechanisms and Comparisons with Bone Marrow Adiposity

              Skeletal muscle and bone share common embryological origins from mesodermal cell populations and also display common growth trajectories early in life. Moreover, muscle and bone are both mechanoresponsive tissues, and the mass and strength of both tissues decline with age. The decline in muscle and bone strength that occurs with aging is accompanied in both cases by an accumulation of adipose tissue. In bone, adipocyte (AC) accumulation occurs in the marrow cavities of long bones and is known to increase with estrogen deficiency, mechanical unloading, and exposure to glucocorticoids. The factors leading to accumulation of intra- and intermuscular fat (myosteatosis) are less well understood, but recent evidence indicates that increases in intramuscular fat are associated with disuse, altered leptin signaling, sex steroid deficiency, and glucocorticoid treatment, factors that are also implicated in bone marrow adipogenesis. Importantly, accumulation of ACs in skeletal muscle and accumulation of intramyocellular lipid are linked to loss of muscle strength, reduced insulin sensitivity, and increased mortality among the elderly. Resistance exercise and whole body vibration can prevent fatty infiltration in skeletal muscle and also improve muscle strength. Therapeutic strategies to prevent myosteatosis may improve muscle function and reduce fall risk in the elderly, potentially impacting the incidence of bone fracture.
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                Author and article information

                Journal
                J Clin Med
                J Clin Med
                jcm
                Journal of Clinical Medicine
                MDPI
                2077-0383
                01 April 2021
                April 2021
                : 10
                : 7
                : 1404
                Affiliations
                [1 ]Department of Orofacial Pain and Oral Medicine, Kyung Hee University Dental Hospital, #613 Hoegi-dong, Dongdaemun-gu, Seoul 02447, Korea; dental21@ 123456khu.ac.kr
                [2 ]Department of Radiology, Kyung Hee University College of Medicine, Kyung Hee University Hospital, #26 Kyunghee-daero, Dongdaemun-gu, Seoul 02447, Korea; oralmedicine@ 123456khu.ac.kr
                Author notes
                [* ]Correspondence: omod0209@ 123456gmail.com ; Tel.: +82-2-958-9409; Fax: +82-2-968-0588
                Author information
                https://orcid.org/0000-0001-7323-0411
                Article
                jcm-10-01404
                10.3390/jcm10071404
                8036470
                33915742
                ecbae797-2218-4da8-87dc-07f35ff59923
                © 2021 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( https://creativecommons.org/licenses/by/4.0/).

                History
                : 02 March 2021
                : 29 March 2021
                Categories
                Article

                whiplash injury,temporomandibular disorder,magnetic resonance imaging,masticatory muscle,lateral pterygoid muscle,masseter muscle

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