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1.
Arch Oral Biol ; 110: 104599, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31734543

RESUMO

OBJECTIVE: We aimed to investigate alteration in cellular signaling mediated by vascular endothelial growth factor (VEGF) and parameters of oxidative stress/nitric oxide generation, superoxide dismutase (SOD) and neuronal nitric oxide synthase (nNOS), underlying altered functional mechanical loading of TMJ (temporomandibular joint) during lateral mandibular deviation. DESIGN: Thirty-eight 5-week-old male Wistar rats were divided into experimental group, which received acrylic resin appliance that shifted mandible to the left during closure, and control group. Computed tomography and histomorphometry were used for condyle analyses, while samples of condyle, synovial membrane and m. masseter were analyzed with enzyme-linked immunosorbent assay and spectrophotometry to determine VEGF and nNOS protein concentrations, and SOD activity. RESULTS: Experimental group of rats developed smaller and asymmetrical mandibles. Less of new bone and cartilage formation and larger bone marrow cavities area were found in the experimental group. Higher VEGF expression in condyle and m. masseter as well as higher nNOS expression in m. masseter and synovial membrane were found in the experimental compared to the control group. Alteration of SOD activity was found in m. masseter and synovial membrane in the experimental group. CONCLUSIONS: Lateral mandibular deviation induces mandibular and condylar morphological changes as well as significant cellular signaling alterations in condyle, synovial membrane and masticatory muscle. Cellular VEGF protein overexpression and oxidative stress/nitric oxide disbalance could be the mechanisms underlying unbalanced functional TMJ loading due to mandibular deviation.


Assuntos
Côndilo Mandibular , Músculo Masseter , Estresse Oxidativo , Membrana Sinovial , Fator A de Crescimento do Endotélio Vascular , Animais , Masculino , Mandíbula/metabolismo , Côndilo Mandibular/metabolismo , Músculo Masseter/metabolismo , Óxido Nítrico , Ratos , Ratos Wistar , Membrana Sinovial/metabolismo , Fator A de Crescimento do Endotélio Vascular/metabolismo
2.
Ann Anat ; 224: 117-123, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31117003

RESUMO

Specific ultrastructural anatomy of masticatory muscles is commonly referred to a general pattern assigned to striated muscles. Junctional feet consisting of calcium channels of the sarcoplasmic reticulum (i.e. the ryanodine receptors, RyRs) physically connected to the calcium channels of the t-tubules build triads within striated muscles. Functional RyRs were demonstrated in the nuclear envelopes of pancreas and of a skeletal muscle derived cell line, but not in muscle in situ. It was hypothesized that ryanodine receptors (RyRs) could also exist in the nuclear envelope in the masseter muscle, thus aiming at studying this by transmission electron microscopy. There were identified paired and consistent subsarcolemmal clusters of mitochondria, appearing as outpockets of the muscle fibers, usually flanking an endomysial microvessel. It was observed on grazing longitudinal cuts that the I-band-limited mitochondria were not strictly located in a single intermyofibrillar space but continued transversally over the I-band to the next intermyofibrillar space. It appeared that the I-band-limited transverse mitochondria participate with the column-forming mitochondria in building a rather incomplete mitochondrial reticulum of the masseter muscle. Subsarcolemmal nuclei presented nuclear envelope-associated RyRs. Moreover, t-tubules were contacting the nuclear envelope and they were seemingly filled from the perinuclear space. This could suggest that nucleoplasmic calcium could contribute to balance the cytosolic concentration via pre-built anatomical routes: (i) indirectly, via the RyRs of the nuclear envelope and (ii) directly via the communication of t-tubules and sarcoplasmic reticulum through the perinuclear space.


Assuntos
Cálcio/metabolismo , Músculo Masseter/metabolismo , Músculo Masseter/ultraestrutura , Animais , Núcleo Celular/ultraestrutura , Masculino , Microscopia Eletrônica de Transmissão , Microvasos/ultraestrutura , Mitocôndrias/ultraestrutura , Modelos Animais , Fibras Musculares Esqueléticas/ultraestrutura , Miofibrilas/ultraestrutura , Membrana Nuclear/ultraestrutura , Coelhos , Sarcolema/ultraestrutura , Sarcômeros/ultraestrutura
3.
Neurosci Lett ; 698: 180-185, 2019 04 17.
Artigo em Inglês | MEDLINE | ID: mdl-30639512

RESUMO

Although the effects of neprilysin (NEP), also called CD10, on the clearance of Alzheimer's disease (AD)-associated amyloid-ß (Aß) have been reported, NEP is not made in the brain, and the mechanism for the transport of NEP to the brain has not been investigated. Our hypothesis is that muscle packages NEP in exosomes in response to a neuromuscular signal and sends it to the brain via retrograde axonal transport. The masseter muscle (MM) and the trigeminal nerve (TGN) are good candidates for this mechanism by virtue of their proximity to the brain. The aim of this study was to trace the NEP protein from the MM, through the TGN, and to the hippocampus (HPC) in muscle contraction models in vitro and in vivo. NEP expression in mouse tissue lysates was analyzed by RT-PCR and Western blot. Four-week-old mice were perfused to remove blood NEP contamination. The MM expressed substantial levels of NEP protein and mRNA. On the other hand, a remarkably high level of NEP protein was measured in the TGN in the absence of mRNA. NEP protein, without the corresponding mRNA, was also detected in the HPC. These results suggested that the MM derived NEP was taken up by the TGN, which in turn permitted NEP access to the central nervous system and within it the HPC. When the MM was induced to contract by electric stimulation in freshly euthanized mice, NEP protein decreased in the MM in a stimulus time-dependent manner, while that in the TGN and the HPC increased sequentially. Furthermore, NIR-labeled exosomes tracked along the same route. Finally, carbachol induced secretion of exosomal NEP in C2C12-derived myotube cells. These results support our hypothesis that MM-derived NEP is transported along the TGN to reach the HPC following electrical or cholinergic stimulation.


Assuntos
Peptídeos beta-Amiloides/metabolismo , Hipocampo/metabolismo , Músculo Masseter/metabolismo , Neprilisina/metabolismo , Doença de Alzheimer/genética , Precursor de Proteína beta-Amiloide/genética , Animais , Encéfalo/metabolismo , Modelos Animais de Doenças , Masculino , Camundongos Endogâmicos C57BL , Neurônios/metabolismo
4.
Nan Fang Yi Ke Da Xue Xue Bao ; 38(6): 755-760, 2018 Jun 20.
Artigo em Chinês | MEDLINE | ID: mdl-29997101

RESUMO

OBJECTIVE: To investigate the changes in mitochondrial calcium and extracellular sodium concentrations in the masseter muscle of rats with occlusal interference and the regulatory mechanism of mitochondrial Ca2+ overload by calmodulin kinase II (CaMK II). METHODS: SD rat models of occlusal interference were established by placing a stainless steel segments (0.8 mm in diameter) to raise the occlusal surface of the upper right first molar. At 3, 7, 14, and 21 days after occlusal interference and at 3 days after removal of occlusal interference, HE staining was used to observe the histomorphological changes of the masseter muscle. Mitochondrial calcium concentration in the masseter muscle was detected using fluorescence spectrophotometry, and direct turbidimetry with potassium pyroantimonate was used to detect the extracellular sodium concentration; the expression levels of masseter muscle p-CaMK II (Thr287) and CaMK II were detected using Western blotting. RESULTS: Compared with those in the corresponding control groups, mitochondrial Ca2+ concentration in the masseter muscle on occlusal interference side increased significantly at 3, 7, 14 and 21 days after occlusal interference (P<0.05), but was significantly lowered at 3 days after removal of the interference (P<0.05). The concentration of extracellular Na+ increased progressively with time at 3, 7, 14 and 21 days after occlusal interference (P<0.05), and was significantly decreased at 3 days after interference removal (P<0.05). Occlusal interference for 3, 7 and 14 days resulted in significantly increased expressions of p-CaMK II (Thr287) and CaMK II (P<0.05), which was significantly decreased at 21 days compared with those in the control groups (P<0.05) and further decreased after removal of occlusal interference (P<0.05). Similar changes were also observed on the side without interference, but the changes on the interference side were more obvious (P<0.05). CONCLUSION: Occlusal interference causes elevated mitochondrial Ca2+ and extracellular Na+ concentrations in the masseter muscle of rats to lead to calcium overload; the increase in mitochondrial Ca2+ concentration is correlated with the phosphorylation level of CaMK II signaling pathway, suggesting a negative feedback regulation mechanism by the CaMK II signal pathway.


Assuntos
Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina/metabolismo , Cálcio/metabolismo , Má Oclusão/metabolismo , Músculo Masseter/metabolismo , Mitocôndrias Musculares/metabolismo , Sódio/metabolismo , Animais , Retroalimentação Fisiológica , Ratos , Ratos Sprague-Dawley
5.
Neuroscience ; 384: 290-299, 2018 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-29890293

RESUMO

Craniofacial muscle pain, such as spontaneous pain and bite-evoked pain, are major symptoms in patients with temporomandibular disorders and infection. However, the underlying mechanisms of muscle pain, especially mechanisms of highly prevalent spontaneous pain, are poorly understood. Recently, we reported that transient receptor potential vanilloid 1 (TRPV1) contributes to spontaneous pain but only marginally contributes to bite-evoked pain during masseter inflammation. Here, we investigated the role of transient receptor potential ankyrin 1 (TRPA1) in spontaneous and bite-evoked pain during masseter inflammation, and dissected the relative contributions of TRPA1 and TRPV1. Masseter inflammation increased mouse grimace scale (MGS) scores and face wiping behaviors. Pharmacological or genetic inhibition of TRPA1 significantly attenuated MGS but not face wiping behaviors. MGS scores were also attenuated by scavenging putative endogenous ligands for TRPV1 or TRPA1. Simultaneous inhibition of TRPA1 by AP18 and TRPV1 by AMG9810 in masseter muscle resulted in robust inhibition of both MGS and face wiping behaviors. Administration of AP18 or AMG9810 to masseter muscle induced conditioned place preference (CPP). The extent of CPP following simultaneous administration of AP18 and AMG9810 was greater than that induced by the individual antagonists. In contrast, inflammation-induced reduction of bite force was not affected by the inhibition of TRPA1 alone or in combination with TRPV1. These results suggest that simultaneous inhibition of TRPV1 and TRPA1 produces additive relief of spontaneous pain, but does not ameliorate bite-evoked pain during masseter inflammation. Our results provide further evidence that distinct mechanisms underlie spontaneous and bite-evoked pain from inflamed masseter muscle.


Assuntos
Inflamação/metabolismo , Músculo Masseter/metabolismo , Mialgia/metabolismo , Canal de Cátion TRPA1/metabolismo , Canais de Cátion TRPV/metabolismo , Acrilamidas/farmacologia , Animais , Comportamento Animal/efeitos dos fármacos , Compostos Bicíclicos Heterocíclicos com Pontes/farmacologia , Condicionamento Operante/efeitos dos fármacos , Músculo Masseter/efeitos dos fármacos , Camundongos , Oximas/farmacologia , Medição da Dor , Canal de Cátion TRPA1/antagonistas & inibidores , Canais de Cátion TRPV/antagonistas & inibidores
6.
Exp Cell Res ; 371(1): 20-30, 2018 10 01.
Artigo em Inglês | MEDLINE | ID: mdl-29842877

RESUMO

Although resident cardiac stem cells have been reported, regeneration of functional cardiomyocytes (CMs) remains a challenge. The present study identifies an alternative progenitor source for CM regeneration without the need for genetic manipulation or invasive heart biopsy procedures. Unlike limb skeletal muscles, masseter muscles (MM) in the mouse head are developed from Nkx2-5 mesodermal progenitors. Adult masseter muscle satellite cells (MMSCs) display heterogeneity in developmental origin and cell phenotypes. The heterogeneous MMSCs that can be characterized by cell sorting based on stem cell antigen-1 (Sca1) show different lineage potential. While cardiogenic potential is preserved in Sca1+ MMSCs as shown by expression of cardiac progenitor genes (including Nkx2-5), skeletal myogenic capacity is maintained in Sca1- MMSCs with Pax7 expression. Sca1+ MMSC-derived beating cells express cardiac genes and exhibit CM-like morphology. Electrophysiological properties of MMSC-derived CMs are demonstrated by calcium transients and action potentials. These findings show that MMSCs could serve as a novel cell source for cardiomyocyte replacement.


Assuntos
Diferenciação Celular , Músculo Masseter/citologia , Desenvolvimento Muscular/genética , Miócitos Cardíacos/citologia , Células Satélites de Músculo Esquelético/citologia , Potenciais de Ação/fisiologia , Animais , Ataxina-1/genética , Ataxina-1/metabolismo , Biomarcadores/metabolismo , Cálcio/metabolismo , Linhagem da Célula/genética , Expressão Gênica , Genes Reporter , Proteínas de Fluorescência Verde/genética , Proteínas de Fluorescência Verde/metabolismo , Proteína Homeobox Nkx-2.5/genética , Proteína Homeobox Nkx-2.5/metabolismo , Proteínas Luminescentes/genética , Proteínas Luminescentes/metabolismo , Músculo Masseter/metabolismo , Camundongos , Camundongos Transgênicos , Miócitos Cardíacos/metabolismo , Fator de Transcrição PAX7/genética , Fator de Transcrição PAX7/metabolismo , Fenótipo , Regeneração , Células Satélites de Músculo Esquelético/metabolismo
7.
Arch Oral Biol ; 91: 103-108, 2018 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-29703519

RESUMO

OBJECTIVE: The jaw-closing muscles of humans and nonprimate mammals express alpha-cardiac fibers but MyHC α-cardiac has not been identified in the jaw adductors of nonhuman primates. We determined whether MyHC α-cardiac is expressed in the superficial masseter and temporalis muscles of the sooty mangabey (Cercocebus atys), an African Old World monkey that specializes on hard seeds. DESIGN: LC-MS/MS based proteomics was used to identify the presence of MyHC Iα. Immunohistochemistry was used to analyze the composition and distribution of fiber types in the superficial masseter and temporalis muscles of eight C. atys. Serial sections were stained against MyHC α-cardiac (MYH6), as well as MyHC-1 (NOQ7.5.4D), MyHC-2 (MY-32), and MyHC-M (2F4). RESULTS: Proteomics analysis identified the presence of Myosin-6 (MyHC α-cardiac) in both heart atrium and superficial masseter. MyHC α-cardiac was expressed in abundance in the superficial masseter and temporalis muscles of all eight individuals and hybrid fibers were common. CONCLUSIONS: The identification of MyHC α-cardiac in the jaw adductors of sooty mangabeys is a novel finding for nonhuman primates. The abundance of MyHC α-cardiac indicates a fatigue-resistant fiber population characterized by intermediate speed of contraction between pure MyHC-1 and MyHC-2 isoforms. We suggest that α-cardiac fibers may be advantageous to sooty mangabeys, whose feeding behavior includes frequent crushing of relatively large, hard seeds during the power stroke of ingestion. Additional studies comparing jaw-adductor fiber phenotype of hard-object feeding primates and other mammals are needed to explore this relationship further.


Assuntos
Imuno-Histoquímica/métodos , Músculo Masseter/metabolismo , Proteômica/métodos , Músculo Temporal/metabolismo , Miosinas Ventriculares/isolamento & purificação , Miosinas Ventriculares/metabolismo , Animais , Cercocebus atys , Feminino , Humanos , Masculino , Músculo Masseter/patologia , Cadeias Pesadas de Miosina/isolamento & purificação , Cadeias Pesadas de Miosina/metabolismo , Primatas , Isoformas de Proteínas , Músculo Temporal/patologia
8.
Ann Anat ; 216: 112-119, 2018 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-29289710

RESUMO

BACKGROUND: Masseter muscle paralysis induced by botulinum toxin type A (BoNTA) evokes subchondral bone loss in mandibular heads of adult rats and growing mice after 4 weeks. However, the primary cellular and molecular events leading to altered bone remodeling remain unexplored. Thus, the aim of the current work has been to assess the molecular response that precedes the early microanatomical changes in the masseter muscle and subchondral bone of the mandibular head in adult mice after BoNTA intervention. METHODS: A pre-clinical in vivo study was performed by a single intramuscular injection of 0.2 U BoNTA in the right masseter (experimental) of adult BALB/c mice. The contralateral masseter was injected with vehicle (control). Changes in mRNA levels of molecular markers of bone loss or muscle atrophy/regeneration were addressed by qPCR at day 2 or 7, respectively. mRNA levels of receptor activator of nuclear factor-κB ligand (RANKL) was assessed in mandibular heads, whilst mRNA levels of Atrogin-1/MAFbx, MuRF-1 and Myogenin were addressed in masseter muscles. In order to identify the early microanatomical changes at day 14, fiber diameters in transversal sections of masseter muscles were quantified, and histomorphometric analysis was used to determine the bone per tissue area and the trabecular thickness of subchondral bone of the mandibular heads. RESULTS: An increase of up to 4-fold in RANKL mRNA levels were detected in mandibular heads of the BoNTA-injected sides as early as 2 days after intervention. Moreover, a 4-6 fold increase in Atrogin-1/MAFbx and MuRF-1 and an up to 25 fold increase in Myogenin mRNA level were detected in masseter muscles 7 days after BoNTA injections. Masseter muscle mass, as well as individual muscle fiber diameter, were significantly reduced in BoNTA-injected side after 14 days post-intervention. At the same time, in the mandibular heads from the treated side, the subchondral bone loss was evinced by a significant reduction in bone per tissue area (-40%) and trabecular thickness (-55%). CONCLUSIONS: Our results show that masseter muscle paralysis induced by BoNTA leads to significant microanatomical changes by day 14, preceded by molecular changes as early as 2 days in bone, and 7 days in muscle. Therefore, masseter muscle atrophy and subchondral bone loss detected at 14 days are preceded by molecular responses that occur during the first week after BoNTA intervention.


Assuntos
Toxinas Botulínicas Tipo A/farmacologia , Côndilo Mandibular/efeitos dos fármacos , Côndilo Mandibular/ultraestrutura , Músculo Masseter/efeitos dos fármacos , Músculo Masseter/ultraestrutura , Fármacos Neuromusculares/farmacologia , Animais , Atrofia , Injeções Intramusculares , Masculino , Côndilo Mandibular/metabolismo , Músculo Masseter/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Proteínas Musculares/biossíntese , Osteoporose/patologia , Paralisia/induzido quimicamente , RNA Mensageiro/análise , RNA Mensageiro/biossíntese
9.
Muscle Nerve ; 57(1): 96-99, 2018 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-28187528

RESUMO

INTRODUCTION: Botulinum neurotoxin A (BoNTA) has long been used as a therapeutic agent and has been widely accepted as a cosmetic agent in recent years. It can inhibit function and induce structural changes in skeletal muscle. METHODS: Specimens of fresh dissected human masseter muscle were used to observe the ultrastructural changes that occurred at 6 and 12 months following BoNTA injection. RESULTS: The findings observed were muscle fiber distortion, sarcomere shortening, mitochondrial vacuolar degeneration, glycogen accumulation, and H and M band disruption in the triad of tubules. At 12 months after injection, there was still evidence of degenerative changes in muscle ultrastructure, whereas most organelles exhibited a normal structure. DISCUSSION: Profound ultrastructural and organelle disfiguring changes were observed after BoNTA injection into human masseter muscle. Most changes were transient, however, and were resolved by 12 months after injection. Muscle Nerve 57: 96-99, 2018.


Assuntos
Toxinas Botulínicas Tipo A/farmacologia , Músculo Masseter/efeitos dos fármacos , Músculo Masseter/ultraestrutura , Fármacos Neuromusculares/farmacologia , Adulto , Grupo com Ancestrais do Continente Asiático , Toxinas Botulínicas Tipo A/administração & dosagem , Face/anatomia & histologia , Feminino , Glicogênio/metabolismo , Humanos , Injeções Intramusculares , Músculo Masseter/metabolismo , Microscopia Eletrônica , Microtúbulos/metabolismo , Microtúbulos/patologia , Mitocôndrias Musculares/efeitos dos fármacos , Mitocôndrias Musculares/ultraestrutura , Fibras Musculares Esqueléticas/efeitos dos fármacos , Fibras Musculares Esqueléticas/ultraestrutura , Fármacos Neuromusculares/administração & dosagem , Sarcômeros/efeitos dos fármacos , Sarcômeros/ultraestrutura , Cirurgia Plástica , Adulto Jovem
10.
J Neurosci Res ; 96(6): 1043-1055, 2018 06.
Artigo em Inglês | MEDLINE | ID: mdl-29265492

RESUMO

Calcitonin gene-related peptide (CGRP) is released by motor neurons and affects skeletal muscle fiber and transient receptor potential cation channel subfamily V member 1 (TRPV1), an important marker of pain modulation. However, the expression of CGRP and TRPV1 in the trigeminal ganglion (TG) during changes and in feeding patterns has not been described. We used real-time reverse transcription polymerase chain reaction and in situ hybridization to investigate the mRNA expression levels of CGRP and TRPV1 in the TG. The expression of myosin heavy-chain (MyHC) isoforms was also investigated in the masseter muscle (MM) during the transition from sucking to mastication, an important functional trigger for muscle. The mRNA and protein levels of CGRP increased in the MM and TG from postnatal day 10 (P10) to P20 in male mice. The protein levels of TRPV1 were almost constant in the TG from P10 to P20, in contrast to increases in the MM. The mRNA abundance of TRPV1 in the TG and MM was increased from P10 to P20. The localization of an antisense probe was used to count CGRP cell numbers and found to differentiate the ophthalmic, maxillary, and mandibular nerve divisions of the TG. In particular, the number of CGRP+ cells per 10,000 µm2 in the maxillary and mandibular divisions of the TG gradually changed from P10 to P20. The expression of CGRP and TRPV1 in the TG and MM and the patterns of expression of different MyHC isoforms were affected by changes in feeding during male mouse development.


Assuntos
Músculo Masseter/metabolismo , Neurotransmissores/biossíntese , Gânglio Trigeminal/metabolismo , Animais , Peptídeo Relacionado com Gene de Calcitonina/biossíntese , Peptídeo Relacionado com Gene de Calcitonina/genética , Peptídeo Relacionado com Gene de Calcitonina/metabolismo , Feminino , Hibridização In Situ , Masculino , Camundongos , Cadeias Pesadas de Miosina/metabolismo , Neurotransmissores/genética , Neurotransmissores/metabolismo , Miosina não Muscular Tipo IIB/metabolismo , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Canais de Cátion TRPV/biossíntese , Canais de Cátion TRPV/genética , Canais de Cátion TRPV/metabolismo
11.
Neurochem Int ; 119: 159-170, 2018 10.
Artigo em Inglês | MEDLINE | ID: mdl-29061384

RESUMO

Dystonia musculorum (dt) mice, which have a mutation in the Dystonin (Dst) gene, are used as animal models to investigate the human disease known as hereditary sensory and autonomic neuropathy type VI. Massive neuronal cell death is observed, mainly in the peripheral nervous system (PNS) of dt mice. We and others have recently reported a histopathological feature of these mice that neurofilament (NF) accumulates in various areas of the central nervous system (CNS), including motor pathways. Although dt mice show motor disorder and growth retardation, the causes for these are still unknown. Here we performed histopathological analyses on motor units of the trigeminal motor nucleus (Mo5 nucleus), because they are a good system to understand neuronal responses in the mutant CNS, and abnormalities in this system may lead to problems in mastication, with subsequent growth retardation. We report that motoneurons with NF accumulation in the Mo5 nuclei of DstGt homozygous mice express the stress-induced genes CHOP, ATF3, and lipocalin 2 (Lcn2). We also show a reduced number of Mo5 motoneurons and a reduced size of Mo5 nuclei in DstGt homozygous mice, possibly due to apoptosis, given the presence of cleaved caspase 3-positive Mo5 motoneurons. In the mandibular (V3) branches of the trigeminal nerve, which contains axons of Mo5 motoneurons and trigeminal sensory neurons, there was infiltration of Iba1-positive macrophages. Finally, we report atrophy of the masseter muscles in DstGt homozygous mice, which showed abnormal nuclear localization of myofibrils and increased expression of atrogin-1 mRNA, a muscle atrophy-related gene and weaker masseter muscle strength with uncontrolled muscle activity by electromyography (EMG). Taken together, our findings strongly suggest that mastication in dt mice is affected due to abnormalities of Mo5 motoneurons and masseter muscles, leading to growth retardation at the post-weaning stages.


Assuntos
Axônios/metabolismo , Distonia/metabolismo , Músculo Masseter/metabolismo , Proteínas do Tecido Nervoso/metabolismo , Núcleo Motor do Nervo Trigêmeo/metabolismo , Animais , Proteínas de Transporte/metabolismo , Proteínas do Citoesqueleto/metabolismo , Camundongos Transgênicos , Neurônios Motores/metabolismo , Células Receptoras Sensoriais/metabolismo
12.
J Oral Facial Pain Headache ; 32(1): 75­83, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29145524

RESUMO

AIMS: To determine the involvement of tumor necrosis factor alpha (TNFα) signaling in the trigeminal ganglion (TG) in the mechanical hypersensitivity of the masseter muscle during temporomandibular joint (TMJ) inflammation. METHODS: A total of 55 male Sprague-Dawley rats were used. Following injection of Complete Freund's Adjuvant into the TMJ, the mechanical sensitivities of the masseter muscle and the overlying facial skin were measured. Satellite glial cell (SGC) activation and TNFα expression in the TG were investigated immunohistochemically, and the effects of their inhibition on the mechanical hypersensitivity of the masseter muscle were also examined. Student t test or two-way repeated-measures analysis of variance followed by Bonferroni multiple comparisons test were used for statistical analyses. P < .05 was considered to reflect statistical significance. RESULTS: Mechanical allodynia in the masseter muscle was induced without any inflammatory cell infiltration in the muscle after TMJ inflammation. SGC activation and an increased number of TNFα-immunoreactive cells were induced in the TG following TMJ inflammation. Intra-TG administration of an inhibitor of SGC activity or of TNFα-neutralizing antibody depressed both the increased number of TG cells encircled by activated SGCs and the mechanical hypersensitivity of the masseter following TMJ inflammation. CONCLUSION: These findings suggest that persistent masseter hypersensitivity associated with TMJ inflammation was mediated by SGC-TG neuron interactions via TNFα signaling in the TG.


Assuntos
Músculo Masseter/metabolismo , Transtornos da Articulação Temporomandibular/metabolismo , Gânglio Trigeminal/metabolismo , Fator de Necrose Tumoral alfa/metabolismo , Animais , Anticorpos Neutralizantes , Modelos Animais de Doenças , Adjuvante de Freund , Inflamação/induzido quimicamente , Masculino , Mecanotransdução Celular , Dor/etiologia , Estimulação Física , Ratos , Ratos Sprague-Dawley , Articulação Temporomandibular/metabolismo , Transtornos da Articulação Temporomandibular/induzido quimicamente , Fator de Necrose Tumoral alfa/antagonistas & inibidores
13.
Cranio ; 36(5): 286-293, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-28920539

RESUMO

OBJECTIVE: The aim of this study was to evaluate, quantitatively, the volumetric effects of stabilization splint therapy on the masseter muscle of sleep bruxism (SB) patients. METHODS: The magnetic resonance (MR) images of 16 SB patients diagnosed by polysomnography (PSG) who used stabilization splints for four months were obtained before and after the therapy. The masseter muscle volume was calculated using Cavalieri's principle on the MR images. RESULTS: After the splint therapy, the mean volume of the masseter muscle did not reduce significantly. The fat and/or water content of the muscles did not change either. DISCUSSION: The stabilization splint therapy had no effect on the volume, fat and/or water content of the masseter muscle; however the discomfort was reduced in the patients. Although the effect of splint therapy is not fully understood, the non-invasive and reversible stabilization splint can be used in SB patients because of its relaxation effect on muscles.


Assuntos
Músculo Masseter/patologia , Placas Oclusais , Bruxismo do Sono/patologia , Bruxismo do Sono/terapia , Tecido Adiposo/metabolismo , Água Corporal/metabolismo , Feminino , Humanos , Imagem por Ressonância Magnética , Masculino , Músculo Masseter/diagnóstico por imagem , Músculo Masseter/metabolismo , Bruxismo do Sono/diagnóstico por imagem
14.
Eur J Oral Sci ; 125(6): 453-462, 2017 12.
Artigo em Inglês | MEDLINE | ID: mdl-29105170

RESUMO

This study aimed to investigate the effect of glutamate-evoked masseter muscle pain on intramuscular oxygenation during rest and sustained elevated muscle activity (SEMA). Seventeen healthy individuals participated in two sessions in which they were injected with glutamate and saline in random order. Each session was divided into three, 10-min periods. During the first (period 1) and the last (period 3) 10-min periods, participants performed five intercalated 1-min bouts of masseter SEMA with 1-min periods of 'rest'. At onset of the second 10-min period, glutamate (0.5 ml, 1 M; Ajinomoto, Tokyo, Japan) or isotonic saline (0.5 ml; 0.9%) was injected into the masseter muscle and the participants kept the muscle relaxed in a resting position for 10 min (period 2). The hemodynamic characteristics of the masseter muscle were recorded simultaneously during the experiment by a laser blood-oxygenation monitor. The results demonstrated that glutamate injections caused significant levels of self-reported pain in the masseter muscle; however, this nociceptive input did not have robust effects on intramuscular oxygenation during rest or SEMA tasks. Interestingly, these findings suggest an uncoupling between acute nociceptive activity and hemodynamic parameters in both resting and low-level active jaw muscles. Further studies are needed to explore the pathophysiological significance of blood-flow changes for persistent jaw-muscle pain conditions.


Assuntos
Ácido Glutâmico/farmacologia , Músculo Masseter/efeitos dos fármacos , Músculo Masseter/metabolismo , Contração Muscular/efeitos dos fármacos , Oxigênio/sangue , Adulto , Feminino , Voluntários Saudáveis , Hemodinâmica , Humanos , Masculino , Medição da Dor , Limiar da Dor
15.
Eur J Pain ; 21(10): 1732-1742, 2017 11.
Artigo em Inglês | MEDLINE | ID: mdl-28722246

RESUMO

BACKGROUND: This study investigated whether intramuscular injection of delta-9-tetrahydrocannabinol (THC), by acting on peripheral cannabinoid (CB) receptors, could decrease nerve growth factor (NGF)-induced sensitization in female rat masseter muscle; a model which mimics the symptoms of myofascial temporomandibular disorders. METHODS: Immunohistochemistry was used to explore the peripheral expression of cannabinoid receptors in the masseter muscle while behavioural and electrophysiology experiments were employed to assess the functional effects of intramuscular injection of THC. RESULTS: It was found that CB1 and CB2 receptors are expressed by trigeminal ganglion neurons that innervate the masseter muscle and also on their peripheral endings. Their expression was greater in TRPV1-positive ganglion neurons. Three days after intramuscular injection of NGF, ganglion neuron expression of CB1 and CB2, but not TPRV1, was decreased. In behavioural experiments, intramuscular injection (10 µL) of THC (1 mg/mL) attenuated NGF-induced mechanical sensitization. No change in mechanical threshold was observed in the contralateral masseter muscles and no impairment of motor function was found after intramuscular injections of THC. In anaesthetized rats, the same concentration of THC increased the mechanical thresholds of masseter muscle mechanoreceptors. Co-administration of the CB1 antagonist AM251 blocked the effect of THC on masseter muscle mechanoreceptors while the CB2 antagonist AM630 had no effect. CONCLUSIONS: These results suggest that reduced inhibitory input from the peripheral cannabinoid system may contribute to NGF-induced local myofascial sensitization of mechanoreceptors. Peripheral application of THC may counter this effect by activating the CB1 receptors on masseter muscle mechanoreceptors to provide analgesic relief without central side effects. SIGNIFICANCE: Our results suggest THC could reduce masticatory muscle pain through activating peripheral CB1 receptors. Peripheral application of cannabinoids could be a novel approach to provide analgesic relief without central side effects.


Assuntos
Agonistas de Receptores de Canabinoides/uso terapêutico , Dronabinol/uso terapêutico , Músculo Masseter/metabolismo , Síndromes da Dor Miofascial/tratamento farmacológico , Receptor CB1 de Canabinoide/metabolismo , Receptor CB2 de Canabinoide/metabolismo , Animais , Modelos Animais de Doenças , Feminino , Músculo Masseter/fisiopatologia , Mecanorreceptores , Síndromes da Dor Miofascial/etiologia , Síndromes da Dor Miofascial/metabolismo , Fator de Crescimento Neural , Neurônios/metabolismo , Ratos , Ratos Sprague-Dawley , Gânglio Trigeminal/metabolismo
16.
Arch Oral Biol ; 83: 63-67, 2017 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-28719832

RESUMO

OBJECTIVE: The aim of this study is to examine the expression pattern of the different myosin heavy chain (MyHC) isoforms in the masseter and medial pterygoid muscles by real time quantitative polymerase chain reaction (RT-qPCR) to obtain information at molecular level which can be related to the functional characteristics of these two muscles. DESIGN: The masseter, deep and superficial portion, and medial pterygoid muscles of five adult Pan troglodytes were dissected in order to obtain samples of the anterior and posterior regions of each portion of the masseter and of the medial pterygoid. The expression of MyHC isoforms mRNA transcripts was analyzed by RT-qPCR. RESULTS: No significant differences in expression of MyHC isoforms between the masseter and the medial pterygoid were found. In contrast, when comparing the superficial and the deep portion of the masseter, we found that the MyHC-IIM isoform was expressed at a significantly higher level in the superficial portion. CONCLUSIONS: The superficial portion of the masseter and the medial pterygoid muscle have the same expression pattern regarding the different MyHC isoforms. On the other hand, the deep portion of the masseter, which is activated mainly during lateral and repositioning movements of the mandible, has a lower MyHC-IIM isoform expression than the superficial portion. Our findings provide new data on functional aspects of the masseter and medial pterygoid that can complement results obtained by other techniques.


Assuntos
Músculo Masseter/metabolismo , Cadeias Pesadas de Miosina/metabolismo , Músculos Pterigoides/metabolismo , Isoformas de RNA/metabolismo , Animais , Pan troglodytes , Reação em Cadeia da Polimerase em Tempo Real
17.
J Pain ; 18(11): 1333-1345, 2017 11.
Artigo em Inglês | MEDLINE | ID: mdl-28669862

RESUMO

Spontaneous pain and function-associated pain are prevalent symptoms of multiple acute and chronic muscle pathologies. We established mouse models for evaluating spontaneous pain and bite-evoked pain from masseter muscle, and determined the roles of transient receptor potential cation channel subfamily V member 1 (TRPV1) and the contribution of TRPV1- or neurokinin 1 (NK1)-dependent nociceptive pathways. Masseter muscle inflammation increased Mouse Grimace Scale scores and face-wiping behavior, which were attenuated by pharmacological or genetic inhibition of TRPV1. Masseter inflammation led to a significant reduction in bite force. Inhibition of TRPV1 only marginally relieved the inflammation-induced reduction of bite force. These results suggest a differential extent of contribution of TRPV1 to the 2 types of muscle pain. However, chemical ablation of TRPV1-expressing nociceptors or chemogenetic silencing of TRPV1-lineage nerve terminals in masseter muscle attenuated inflammation-induced changes in Mouse Grimace Scale scores as well as bite force. Furthermore, ablation of neurons expressing NK1 receptor in trigeminal subnucleus caudalis also prevented both types of muscle pain. Our results suggest that TRPV1 differentially contributes to spontaneous pain and bite-evoked muscle pain, but TRPV1-expressing afferents and NK1-expressing second-order neurons commonly mediate both types of muscle pain. Therefore, manipulation of the nociceptive circuit may provide a novel approach for management of acute or chronic craniofacial muscle pain. PERSPECTIVE: We report the profound contribution of TRPV1 to spontaneous muscle pain but not to bite-evoked muscle pain. These 2 types of muscle pain are transmitted through a common nociceptive pathway. These results may help to develop new strategies to manage multiple modes of muscle pain simultaneously by manipulating pain circuits.


Assuntos
Dor Facial/metabolismo , Mialgia/metabolismo , Dor Nociceptiva/metabolismo , Canais de Cátion TRPV/metabolismo , Animais , Força de Mordida , Modelos Animais de Doenças , Dor Facial/etiologia , Dor Facial/patologia , Adjuvante de Freund , Inflamação/metabolismo , Masculino , Músculo Masseter/metabolismo , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Mialgia/etiologia , Mialgia/patologia , Neurônios/metabolismo , Neurônios/patologia , Dor Nociceptiva/etiologia , Dor Nociceptiva/patologia , Pressão , Distribuição Aleatória , Receptores da Neurocinina-1/metabolismo , Canais de Cátion TRPV/genética , Núcleos do Trigêmeo/metabolismo , Núcleos do Trigêmeo/patologia
18.
J Physiol Pharmacol ; 68(2): 181-189, 2017 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-28614767

RESUMO

Progressive muscle wasting, frequently associated with inflammation, muscle fibre degeneration and fibrosis, is a characteristic of DMD (Duchenne muscular dystrophy). Its most common used animal model, the mdx mouse, however can overcome muscle degeneration by regeneration processes and is for this reason not suitable to answer all scientific questions. The aim of this study was to evaluate the ability of botulinum toxin A (BTX-A) in breaking down muscle regeneration in mdx mice. For this purpose, the right masseter muscle of 100 days old mdx and healthy mice was paralyzed by a single specific intramuscular injection of BTX-A. After 21 days, right and left masseter and temporal muscles as well as tongue muscle were carefully dissected, and gene and protein expression of caveolin-1, caveolin-3 and vascular endothelial growth factor (VEGF) were determined using quantitative RT-PCR and Western blot technique. Statistics were performed using Student's t-test and Mann Whitney U-test (significance level: P ≤ 0.05). After BTX-A injection, in both mice strains and for all three studied genes, no significant differences in mRNA amount could be detected between treated and untreated masseter muscles. A significant increase in caveolin-1, caveolin-3 and VEGF mRNA expression could only be found in the right temporal muscle of control mice compared to the left side. All three investigated proteins were more frequent to be found in dystrophic masseter muscle samples compared to the corresponding control samples, whereas significant decreased caveolin-3 protein levels could only be detected in the treated masseter versus untreated masseter muscle of controls. In contrast to previous conclusions, with this study it was not possible to prove a BTX-A-induced dystrophic phenotype in control animals, in which only the known decreases of caveolin-3 protein expression could be verified due to denervation. At the same time, however, gene and protein expression in dystrophic mice was not changed after BTX-A injection.


Assuntos
Toxinas Botulínicas Tipo A/farmacologia , Caveolina 1/metabolismo , Caveolina 3/metabolismo , Músculo Masseter/efeitos dos fármacos , Fator A de Crescimento do Endotélio Vascular/metabolismo , Animais , Caveolina 1/genética , Caveolina 3/genética , Distrofina/deficiência , Feminino , Masculino , Músculo Masseter/metabolismo , Camundongos Endogâmicos C57BL , Camundongos Endogâmicos mdx , RNA Mensageiro/metabolismo , Fator A de Crescimento do Endotélio Vascular/genética
19.
Okajimas Folia Anat Jpn ; 93(4): 127-138, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28637996

RESUMO

The localization of calcitonin gene-related peptide (CGRP) is similar to that of a neurotransmitter which indicates masticatory muscle pain in the area of the masseter fascia. CGRP is released from the trigeminal ganglion (TG). The aim of this study was to analyze the distribution of CGRP in the fascia of the masseter muscle (FMM) and TG in a morphometric manner, with respect to the location and density of CGRP-immunopositive reaction fiber (CGRP-IRF). A higher number of the CGRP-IRF were mainly found located around elongated blood vessels and small nerves on the origin side of the middle zone FMM in the O group (presented with occlusion). In the sectional histochemical analysis of the O group, the CGRP-IRF were clearly detected in oval vessels, large elongated vessels and large nerves in contrast with that of the Non-O group (presented with no occlusion) samples. The number of CGRP-immunopositive ganglion cells (CGRP-IPGCs) in the O group mandibular nerve division was higher than that of other divisions. A reduction of the CGRP-IRF numbers were found in the no-loading groups. The characterization of these locations of CGRP-IPGCs can also provide useful data for the understanding of myofascial pain syndrome of the masseter muscle (MM).


Assuntos
Peptídeo Relacionado com Gene de Calcitonina/metabolismo , Músculo Masseter/metabolismo , Síndromes da Dor Miofascial/metabolismo , Gânglio Trigeminal/metabolismo , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino
20.
J Anesth ; 31(2): 307-317, 2017 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-28246924

RESUMO

Malignant hyperthermia (MH) can be fatal if the crisis is not appropriately treated. It is an inherited disease usually triggered by the administration of volatile inhalational anesthetics and/or succinylcholine, a muscle relaxant. In a patient with suspected MH, the mechanism of calcium release from storage in the sarcoplasmic reticulum in the skeletal muscle is abnormally accelerated. Unexplained hypercarbia representing >55 mmHg of end-tidal carbon dioxide, tachycardia, and muscle rigidity (including masseter muscle rigidity) are early signs of the initiation of MH, because the metabolism is accelerated. The body temperature can rise by >0.5 °C/15 min and may reach ≥40 °C. Respiratory and metabolic acidosis, arrhythmia, cola-colored urine, increased levels of serum potassium, and tented T-waves on electrocardiogram are common and can lead to cardiac arrest. MH should be treated by discontinuation of the triggering agents, administration of intravenous dantrolene (initially 1 mg/kg), and reduction of the body temperature. Early diagnosis and sufficient dantrolene with body temperature reduction are essential to relieve the patient's MH crisis. This guideline in Japanese translation has been posted on the website: http://www.anesth.or.jp/guide/pdf/guideline_akuseikounetsu.pdf .


Assuntos
Temperatura Corporal , Dantroleno/administração & dosagem , Hipertermia Maligna/terapia , Acidose/terapia , Anestésicos Inalatórios/administração & dosagem , Anestésicos Inalatórios/efeitos adversos , Cálcio/metabolismo , Dióxido de Carbono/metabolismo , Humanos , Hipercapnia/complicações , Músculo Masseter/metabolismo , Músculo Esquelético/metabolismo , Retículo Sarcoplasmático/metabolismo , Succinilcolina/administração & dosagem , Succinilcolina/efeitos adversos , Taquicardia/tratamento farmacológico
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