Muscular Dysfunction Research Articles

Immediate and Acute Effect of Self Myofascial Release vs Instrument Assisted Soft Tissue Mobilization on Flexibility, Strength and Sport-Specific Performance in Young Male Soccer Players

Background: Regular exercise and performance can result in microtrau-ma, which is minor damage to the muscle. The resulting inflammatory response may lead to fascia scar tissue over time, which in turn may lead to muscular dysfunction. Purpose: The purpose of our study was to compare the immediate and acute effects of SMR and IASTM on flexibility, strength and sport-specific performance in young male soccer players. Method: Twenty-seven young male soccer players were randomly assigned to receive either SMR via plain foam roller or IASTM via M2T blade. To compare the effect of interventions, subjects were assessed on measures of flexibility via sit and reach test, power through vertical jump test, agility by Illinois agility test, 20m sprint test and strength test by a dynamometer. Results: A one-way ANOVA was used to analyze differences. To test for the difference between interventions and across 3 assessments, a 3X3 split plot ANOVA with a group (control, SMR, IASTM), time (0 min, 10 mins, 20 mins) and interaction effect (Group X Time) was employed. There was a significant difference in strength during performance without intervention vs. immediately after SMR and IASTM (p=0.03). Conclusion: The findings of the study suggest that SMR and IASTM did not improve physical performance in young male soccer players, but they did not hinder performance either. Even if performance does not improve, there does not seem to be any adverse effect by using either SMR or IASTM before physical activity, athletes need not be discouraged from using these tools.

A Review on the Development of Spectroscopic Sensors for the Detection of Creatinine in Human Blood Serum

Creatinine measurement is the key parameter in detecting renal, muscular and thyroid dysfunction. The accurate detection of creatinine level may be informative regarding the functional processes of these systems and help in early detection of acute diseases.There are lots of techniques available for detecting creatinine in human blood serum, most of them are of mainly based on spectroscopic (spectrophotometry, colorimetry and fluorimetric). Other techniques are based on electrochemical, impedometrical, Ion Selective Field-Effect Transistor (ISFET) and chromatography techniques. Each method has its own advantages and few limitations(limitation would be better word) regarding selectivity, sensitivity, reproducibility, cost effective, point-of-care level detection etc. Few methods based on electrochemical techniques are recently promising in detecting creatinine at the point-of-care level with adequate sensitivity and selectivity. On the other hand some biosensors based on spectroscopic techniques are recognized as the most promising substitute in recent years. As creatinine levels in the blood serum offer better information about patient status, here in this review it is thoroughly discussed over other biological samples such as urine, saliva.

The Pathobiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: The Case for Neuroglial Failure.

Although myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) has a specific and distinctive profile of clinical features, the disease remains an enigma because causal explanation of the pathobiological matrix is lacking. Several potential disease mechanisms have been identified, including immune abnormalities, inflammatory activation, mitochondrial alterations, endothelial and muscular disturbances, cardiovascular anomalies, and dysfunction of the peripheral and central nervous systems. Yet, it remains unclear whether and how these pathways may be related and orchestrated. Here we explore the hypothesis that a common denominator of the pathobiological processes in ME/CFS may be central nervous system dysfunction due to impaired or pathologically reactive neuroglia (astrocytes, microglia and oligodendrocytes). We will test this hypothesis by reviewing, in reference to the current literature, the two most salient and widely accepted features of ME/CFS, and by investigating how these might be linked to dysfunctional neuroglia. From this review we conclude that the multifaceted pathobiology of ME/CFS may be attributable in a unifying manner to neuroglial dysfunction. Because the two key features – post exertional malaise and decreased cerebral blood flow – are also recognized in a subset of patients with post-acute sequelae COVID, we suggest that our findings may also be pertinent to this entity.

Tissue Engineering for the Diaphragm and its Various Therapeutic Possibilities – A Systematic Review

AbstractDiaphragmatic impairments exhibit high morbidity as well as mortality while current treatment options remain unsatisfactory. Tissue engineering (TE) approaches have explored the generation of an optimal biocompatible scaffold for diaphragmatic repair through tissue decellularization or de novo construction, with or without the addition of cells. The authors conducted a systematic review on the current state of the art in diaphragmatic tissue engineering (DTE) and found 24 articles eligible for final synthesis. The included approaches studied decellularization‐based graft generation (9) and de novo bioscaffold construction (9). Three studies focused on in vitro host‐scaffold interaction with synthesized, recellularized grafts (2) and decellularized extracellular matrix scaffolds (1). Another three studies investigated evaluation tools for decellularization efficacy. Among all studies, recellularization is performed in both decellularization‐based (4) and de novo generated scaffolds (4). De novo constructed biocomposites as well as decellularized and recellularized scaffolds induced pro‐regenerative remodeling and recovery of diaphragmatic function in all examined animal models. Potential therapeutic applications comprise substance defects requiring patch repair, such as congenital diaphragmatic hernia, and functional diseases demanding an entire organ transplant, like muscular dystrophies or dysfunction after prolonged artificial respiration.

Respiratory and muscular dysfunction of the respiratory muscles and chronic obstructive pulmonary disease: pathophysiological relationships and clinical significance

The review presents literature data on the problem of respiratory muscle (RM) dysfunction in patients with chronic obstructive pulmonary disease (COPD). The main features of their pathophysiological interactions and clinical practice values were observed. Both local and systemic factors of the pathogenesis of COPD are important in the development of RM dysfunction. Local factors are associated with lung remodeling and the need of RM to overcome excessive breathing resistance, which increases the intensity of their work, and contributes to the development of hypertrophy and insufficiency. Chronic systemic inflammation, oxidative stress, excessive proteolysis and other systemic manifestations of COPD change the metabolism, structural and functional organization of RM. The severity of morpho-functional disorders and metabolic status of RM depends on the gravity of COPD and emerges on the early stages as myocytes’ hypertrophy, their increasing capillarization and the increasing of mitochondrion density. At late stages it appears as diffuse replacement of muscle fibers by connective tissue. Low nutritional status, increasing protein-energy deficiency, electrolyte imbalance, endocrine disorders on the background of progressive respiratory insufficiency and tissue hypoxia contribute to the development of RM weakness. The combination of COPD, acute disorders of cerebral circulation and chronic heart failure sharply worsens the function of RM and the prognosis of comorbid diseases. Also, the dysfunction of RM in patients having COPD is significantly aggravated at the age of senility. The review discusses the possibilities of pharmacological correction of RM dysfunction and other clinical aspects of this problem.

Alliance between Malabsorption Syndrome and Hypokalemia in Small Bowel Resection: A Case Report

Introduction: This case will outline the malabsorption syndrome and hypokalemia caused by small bowel resection (S/P anastomosis).SBR avert absorption of nutrients and electrolytes from the small intestine which leads to multiple deficiencies.
 One of the consequences of malabsorption is that the person becomes weak and malnourished. Potassium is necessary for the proper functioning of your muscles, nerves, and heart.
 Low potassium levels have been linked to classic signs and symptoms such as altered mental status, muscular dysfunction and paralysis, and cardiac arrhythmias. One of the first steps in treating patients with non-functioning bowels is to correct electrolyte imbalances. The goal of electrolyte therapy is to prevent complications outside of the gastrointestinal tract. Insufficient digestion and/or absorption of nutritive foods are frequent outcome of significant resection of the digestive tract.
 Malabsorption affects millions of people around the world. Resection of a large portion of the small bowel can result in severe to moderate malabsorption, as well as malnutrition and electrolyte imbalance, as seen in this case.
 The term "malabsorption syndrome" refers to a group of conditions in which the small intestine is unable to absorb enough nutrients and fluids. Macronutrients (carbs, protein, and fats), micronutrients (vitamins and minerals), or both are nutrients that the small intestine has difficulty absorbing.
 Conclusion: The case highlights that small bowel resection induces malabsorption syndrome and hypokalemia in post-operative complication. Hence the physicians need to monitor for the malabsorption signs and symptoms through lab investigations. Further which can be corrected by giving respective treatment and proper diet for the same.
 Keywords: Malabsorption syndrome, hypokalemia , small bowel resection, case report.

Rev1 deficiency induces replication stress to cause metabolic dysfunction differently in males and females.

DNA damage responses compete for cellular resources with metabolic pathways, but little is known about the metabolic consequences of impaired DNA replication, a process called replication stress. Here we characterized the metabolic consequences of DNA replication stress at endogenous DNA lesions by using mice with a disruption of Rev1, a translesion DNA polymerase specialized in the mutagenic replication of damaged DNA. Male and female Rev1 knockout (KO) mice were compared with wild-type (WT) mice and followed over time to study the natural course of body weight gain and glucose tolerance. Follow-up measurements were performed in female mice for in-depth metabolic characterization. Body weight and fat mass were only increased in female KO mice versus WT mice, whereas glucose intolerance and a reduction in lean mass were observed in both sexes. Female KO mice showed reduced locomotor activity while male KO mice showed increased activity as compared with their WT littermates. Further characterization of female mice revealed that lipid handling was unaffected by Rev1 deletion. An increased respiratory exchange ratio, combined with elevated plasma lactate levels and increased hepatic gluconeogenesis indicated problems with aerobic oxidation and increased reliance on anaerobic glycolysis. Supplementation with the NAD+ precursor nicotinamide riboside to stimulate aerobic respiration failed to restore the metabolic phenotype. In conclusion, replication stress at endogenous DNA lesions induces a complex metabolic phenotype, most likely initiated by muscular metabolic dysfunction and increased dependence on anaerobic glycolysis. Nicotinamide riboside supplementation after the onset of the metabolic impairment did not rescue this phenotype.NEW & NOTEWORTHY An increasing number of DNA lesions interferes with cellular replication leading to metabolic inflexibility. We utilized Rev1 knockout mice as a model for replication stress, and show a sex-dependent metabolic phenotype, with a pronounced reduction of lean mass and glucose tolerance. These data indicate that in obesity, we may end up in an infinite loop where metabolic disturbance promotes the formation of DNA lesions, which in turn interferes with cellular replication causing further metabolic disturbances.

Effectiveness of Muscle Energy Technique versus Positional Release Therapy on Range of Motion and Pain in Non-Specific Low Back Pain

Low back ache is the largest cause of sick leave, and half of the population will have experienced a significant incident of low back ache by the age of 30. In India, low back ache prevalence has been reported to be around 23.09%. Severe pain in the lower back is sequel of numerous causes, such as faulty posture, muscular dysfunction (e.g.: muscular imbalance and short or weak muscle), overuse, instability and articular dysfunction in the low back, accident or trauma and most commonly road vehicle accidents. In 85%–90% of cases of lower back ache are non-specific in nature. The function and co-ordination of the muscles that stabilise the lumbar spine, especially the back extensor muscles are often impaired in patients with low back pain. Erector spinae strain and fatigue is one of the causes of back pain. A total of 30 subjects with acute low back pain participated in this study. Group A were treated with hot moist pack and muscle energy technique (MET), whereas Group B were treated with hot moist pack and positional release therapy (PRT). Both the groups received a conventional training protocol for 3 days a week for 4 weeks. The result from these tables shows changes in both the groups, with statistically significant changes were noticed in Group B. The present study showed that both PRT and MET within hot moist packs could be of benefit in the treatment of acute low back pain associated erector spinae muscle spasm. There was significant difference in the intensity of pain within the groups and between the groups after 4 weeks of treatment. Reduction in pain intensity was significant in the PRT group. Pain relief was achieved with both Group A and Group B, but was appreciably more significant in the PRT group. There is a significant difference between both Groups A and B. Hence, PRT is more effective than MET.

The Effects of Passive Stretching Exercise for Sternocleidomastoid(SCM) Muscle on Pulmonary Functions

Purpose : This study aimed to investigate the effect of passive stretching of the sternocleidomastoid(SCM) muscle on pulmonary function. Methods : The subjects were 20 female university students without neurological, muscular, or cardiopulmonary dysfunction. Pulmonary function was tested using a digital pulmonary function-measuring device(Pony FX, COSMED Inc., Italy). The experimental group performed three sets of passive stretching on the SCM muscles. One set included three sets of passive stretching. The control group did not perform any other exercises. After passive stretching, pulmonary function was remeasured. The statistics program was SPSSWIN(ver 25.0) package program. Results : The forced vital capacity(FVC), forced expiratory volume in one second(FEV1), and vital capacity(VC) were significantly improved in the experimental group after stretching exercise. However, there was no change in the control group. The changes in the FVC, FEV1, and maximal voluntary ventilation(MVV) were higher in the experimental group than in the control group. Conclusion : The results indicated that passive stretching exercise of the SCM muscle can improve pulmonary function. In particular, it was particularly effective for maximal effort vital capacity(MEVC) and MVV.

Parathyroid hormone and skeletal muscle cells

Synthetized by the parathyroid glands, parathyroid hormone (PTH) is a single-chain, 84-amino acid polypeptide that controls calcium homeostasis by increasing serum levels, regulating calcium absorption in the small intestine (indirectly thanks to the action of calcitriol), renal reabsorption and removal from the bone matrix. It exerts its classical action mainly by interacting with PTH receptor type 1, a G protein-coupled receptor that is expressed in bone and kidney and activates different signaling pathways. Disorders of the parathyroid glands most commonly present with abnormal serum calcium concentrations: persistent high blood calcium levels are associated with hyperparathyroidism, whereas reduced blood calcium levels are associated with hypoparathyroidism. Both diseases are characterized by muscular dysfunction and myopathies. Even though numerous works suggest an effect of PTH on skeletal muscle, and PTH receptors have been identified in this tissue, knowledge of the cellular and molecular mechanisms of action of this hormone in skeletal muscle is very poor. It is hypothesized that skeletal muscle may be a target for PTH and that its receptors may mediate the effects of PTH. To support these hypotheses and obtain better and more specific understanding for future therapies, it needs to be established, using in vitro cellular models, whether PTH can affect skeletal muscle cell proliferation and differentiation.

Senolytics: A Novel Strategy for Neuroprotection in ALS?

Amyotrophic lateral sclerosis (ALS) is a progressive motor neurodegenerative disease that currently has no cure and has few effective treatments. On a cellular level, ALS manifests through significant changes in the proper function of astrocytes, microglia, motor neurons, and other central nervous system (CNS) cells, leading to excess neuroinflammation and neurodegeneration. Damage to the upper and lower motor neurons results in neural and muscular dysfunction, leading to death most often due to respiratory paralysis. A new therapeutic strategy is targeting glial cells affected by senescence, which contribute to motor neuron degeneration. Whilst this new therapeutic approach holds much promise, it is yet to be trialled in ALS-relevant preclinical models and needs to be designed carefully to ensure selectivity. This review summarizes the pathways involved in ALS-related senescence, as well as known senolytic agents and their mechanisms of action, all of which may inform strategies for ALS-focused drug discovery efforts.

Metformin induces muscle atrophy by transcriptional regulation of myostatin via HDAC6 and FoxO3a

BackgroundSkeletal muscle atrophy is a severe condition that involves loss of muscle mass and quality. Drug intake can also cause muscle atrophy. Biguanide metformin is the first‐line and most widely prescribed anti‐diabetic drug for patients with type 2 diabetes. The molecular mechanism of metformin in muscle is unclear.MethodsMyostatin expression was investigated at the protein and transcript levels after metformin administration. To investigate the pathways associated with myostatin signalling, we used real‐time polymerase chain reaction, immunoblotting, luciferase assay, chromatin immunoprecipitation assay, co‐immunoprecipitation, immunofluorescence, primary culture, and confocal microscopy. Serum analysis, physical performance, and immunohistochemistry were performed using our in vivo model.ResultsMetformin induced the expression of myostatin, a key molecule that regulates muscle volume and triggers the phosphorylation of AMPK. AMPK alpha2 knockdown in the background of metformin treatment reduced the myostatin expression of C2C12 myotubes (−49.86 ± 12.03%, P < 0.01) and resulted in increased myotube diameter compared with metformin (+46.62 ± 0.88%, P < 0.001). Metformin induced the interaction between AMPK and FoxO3a, a key transcription factor of myostatin. Metformin also altered the histone deacetylase activity in muscle cells (>3.12‐fold ± 0.13, P < 0.001). The interaction between HDAC6 and FoxO3a induced after metformin treatment. Confocal microscopy revealed that metformin increased the nuclear localization of FoxO3a (>3.3‐fold, P < 0.001). Chromatin immunoprecipitation revealed that metformin induced the binding of FoxO3a to the myostatin promoter. The transcript‐level expression of myostatin was higher in the gastrocnemius (GC) muscles of metformin‐treated wild‐type (WT) (+68.9 ± 10.01%, P < 0.001) and db/db mice (+55.84 ± 6.62%, P < 0.001) than that in the GC of controls (n = 4 per group). Average fibre cross‐sectional area data also showed that the metformin‐treated C57BL/6J (WT) (−31.74 ± 0.75%, P < 0.001) and C57BLKS/J‐db/db (−18.11 ± 0.94%, P < 0.001) mice had decreased fibre size of GC compared to the controls. The serum myoglobin level was significantly decreased in metformin‐treated WT mice (−66.6 ± 9.03%, P < 0.01).ConclusionsOur results demonstrate that metformin treatment impairs muscle function through the regulation of myostatin in skeletal muscle cells via AMPK‐FoxO3a‐HDAC6 axis. The muscle‐wasting effect of metformin is more evident in WT than in db/db mice, indicating that more complicated mechanisms may be involved in metformin‐mediated muscular dysfunction.

The Application of Exercise Training for Diabetic Peripheral Neuropathy.

Diabetic peripheral neuropathy (DPN) is the presence of symptoms and/or signs of peripheral nerve dysfunction in people with diabetes after the exclusion of other causes. It is associated with pain, paresthesia, sensory loss, muscle atrophy with fat infiltration, and muscular dysfunction typically starting distally in the feet and progressing proximally. Muscle deterioration within the leg and foot can lead to muscle dysfunction, reduced mobility, and increases the risk of disability, ulceration, and amputation. Exercise training is an established method for increasing the different components of physical fitness, including enhancing body composition and improving neuromuscular strength. A number of experimental studies have utilized exercise training to treat various impairments associated with DPN, such as nerve conduction velocity, pain tolerance, and balance. However, the broad spectrum of exercise training modalities implemented and differences in target outcome measurements have made it difficult to understand the efficacy of exercise training interventions or provide appropriate exercise prescription recommendations. Therefore, the aims of this review were to (1) briefly describe the pathophysiology of DPN and (2) discuss the effects of exercise training interventions on sensorimotor, metabolic, and physical functions in people with DPN.

Muscle Physiopathology in Parathyroid Hormone Disorders.

Parathyroid hormone disorders are a group of diseases in which secretion of parathormone (PTH) is impaired. The disorders that result are characterized by signs and symptoms associated with the persistent presence of high blood calcium levels (hypercalcemia) related to hyperparathyroidism (PHPT), or reduced blood calcium levels (hypocalcemia) associated with hypoparathyroidism (HypoPT). In addition to the resulting alteration in bone microarchitecture and mass for both pathologies, patients also report problems with skeletal muscle due to a decrease in muscular strength, muscular dysfunction, and myopathies, which can be responsible for an increased risk of instability and fracture. Although the effect of PTH on bone is well established, and numerous studies suggest that PTH has an effect on skeletal muscle, knowledge about cellular e molecular mechanisms of action on skeletal muscle is very limited. Skeletal muscle is a tissue well known for its structural and mechanical actions and is endowed with an extraordinary ability to adapt to physiological changes. Research in skeletal muscle has increased over the last decade, its importance as an endocrine tissue also emerging, becoming itself a target of numerous substances and hormones. Parathyroid hormone disorders represent a starting point to understand whether PTH may have an effect on skeletal muscle. This review analyzes the basic research data reported to date on PTH and skeletal muscle, highlighting the importance of increasing our knowledge in this field of research.

Acupuncture Efficacy Study Using Electromyographic Signals

Acupuncture is a centuries-old therapeutic technique. However, because of the large number of complicating circumstances, it has been difficult to clearly prove the treatment's therapeutic effectiveness.As a result, acupuncture has failed to acquire acceptance in the mainstream clinical sector. An electromyography (EMG) sensor was built and used to test the efficacy of acupuncture in alleviating muscular stiffness in this study. Electrodes, differential and inverting amplifiers, filters, and a full-wave rectifier made up the EMG circuit. The output of the circuit was sent to a microcontroller for analog-to-digital transformation in order to perform data acquisition. Acupuncture was used to treat four participants who had muscular dysfunction in various regions of their bodies in our case study. Before and after the therapy, EMG signals at the damaged regions were recorded. The findings revealed that the therapy had no immediate conceivable impact on the patients, since the levels of muscular contraction before and after the treatment were comparable. When the EMG signals were measured 30 minutes after the therapy, signs of muscular alleviation were found. This shows that acupuncture does supply patients with beneficial medicine, although slowly. The act of placing the highly conducting needles into the acupuncture sites, we believe, is similar to connecting a parallel wire to a circuit, resulting in a short-circuited route at the meridian. It permits the meridian's polarized in- ner energy, or qi, to pass through. The equilibrium in qi regulation can therefore be restored by unclogging the ow of qi.The repair process is relatively slow, and the treatment impact may not be immediately apparent, because the consti- tutive qualities at the acupuncture points where the needles are pricked may not alter quickly.

Skeletal Muscle Relaxants for the Treatment of Myofascial Pelvic Pain and High Tone Pelvic Floor Disorders in Women: A Scoping Review

Study Objective To review the evidence of muscle relaxants and non-injectable drugs with muscle relaxant properties for the treatment of chronic pelvic pain. This includes investigation of whether the concept of skeletal muscle relaxant use for lower back striated muscle strain is a valid construct to apply to the context and treatment of women with chronic pelvic pain due to myofascial and hypertonic muscular dysfunction. The clinical effectiveness, side effects, and toxicology risk of the investigated drugs were characterized. Design A scoping review was conducted in accordance with PRISMA-ScR guidelines and protocols. Online databases were searched using MeSH and subject terms. Articles reporting evidence on skeletal muscle relaxant use were reviewed by two independent reviewers with a third reviewer for any discrepancies. Setting Scoping review. Patients or Participants N/A. Interventions N/A. Measurements and Main Results Comparison studies have not shown any skeletal muscle relaxant to be superior. Skeletal muscle relaxants are divided into two categories: antispastic and antispasmodic agents. Antispastic agents reduce muscle hypertonicity and involuntary jerks associated with neurological disorders. Antispasmodic agents aim to treat striated muscle spasms from musculoskeletal conditions such as low back pain and myofascial pain. Cyclobenzaprine is heavily studied, with demonstrated effectiveness for isolated conditions. Intravaginal diazepam may be beneficial, while other drugs have limited investigation. Considerable knowledge gaps remain regarding appropriate use of these medications in the context of pelvic pain. Conclusion Scant high-quality data exist to support the use of skeletal muscle relaxants for chronic pelvic pain secondary to myofascial and hypertonic muscular dysfunction. Antispastic agents have limited evidence. Antispasmodic agent usage should be based on side-effect profile, patient preference, abuse potential, and possible drug interactions. Future prospective research on antispasmodic agents in women with myofascial dysfunction is necessary to define medication safety, route, dosage, and clinical outcomes. To review the evidence of muscle relaxants and non-injectable drugs with muscle relaxant properties for the treatment of chronic pelvic pain. This includes investigation of whether the concept of skeletal muscle relaxant use for lower back striated muscle strain is a valid construct to apply to the context and treatment of women with chronic pelvic pain due to myofascial and hypertonic muscular dysfunction. The clinical effectiveness, side effects, and toxicology risk of the investigated drugs were characterized. A scoping review was conducted in accordance with PRISMA-ScR guidelines and protocols. Online databases were searched using MeSH and subject terms. Articles reporting evidence on skeletal muscle relaxant use were reviewed by two independent reviewers with a third reviewer for any discrepancies. Scoping review. N/A. N/A. Comparison studies have not shown any skeletal muscle relaxant to be superior. Skeletal muscle relaxants are divided into two categories: antispastic and antispasmodic agents. Antispastic agents reduce muscle hypertonicity and involuntary jerks associated with neurological disorders. Antispasmodic agents aim to treat striated muscle spasms from musculoskeletal conditions such as low back pain and myofascial pain. Cyclobenzaprine is heavily studied, with demonstrated effectiveness for isolated conditions. Intravaginal diazepam may be beneficial, while other drugs have limited investigation. Considerable knowledge gaps remain regarding appropriate use of these medications in the context of pelvic pain. Scant high-quality data exist to support the use of skeletal muscle relaxants for chronic pelvic pain secondary to myofascial and hypertonic muscular dysfunction. Antispastic agents have limited evidence. Antispasmodic agent usage should be based on side-effect profile, patient preference, abuse potential, and possible drug interactions. Future prospective research on antispasmodic agents in women with myofascial dysfunction is necessary to define medication safety, route, dosage, and clinical outcomes.

Temporomandibular joint disorders in children and adolescent: A review

Temporomandibular disorders (TMD) are a group of joint and muscular dysfunctions affecting the Cranio-orofacial area. Historically, TMDs were once believed to solely affect adults; however, recent studies have discovered an increased prevalence of TMD signs and symptoms in children and adolescents. The reported prevalence of these disorders in pediatric patients varies significantly due to methodological variations among studies; as a result, standardized diagnostic criteria for children are required. In this age group, TMDs can cause pain in the masticatory muscles and TMJs, as well as limited or asymmetric mouth opening and TMJ sounds. Rather than a single causative element, TMDs are produced by a combination of factors such as trauma, occlusion, systemic and developmental problems, and psychological disorders. A complete history and examination, which may include imaging, are essential to obtain a precise diagnosis and assure successful treatment of many disorders. For these issues, there is a range of therapeutic interventions available, although reversible treatments should be favored.

Diverse Roles of Cellular Senescence in Skeletal Muscle Inflammation, Regeneration, and Therapeutics.

Skeletal muscle undergoes vigorous tissue remodeling after injury. However, aging, chronic inflammatory diseases, sarcopenia, and neuromuscular disorders cause muscle loss and degeneration, resulting in muscular dysfunction. Cellular senescence, a state of irreversible cell cycle arrest, acts during normal embryonic development and remodeling after tissue damage; when these processes are complete, the senescent cells are eliminated. However, the accumulation of senescent cells is a hallmark of aging tissues or pathological contexts and may lead to progressive tissue degeneration. The mechanisms responsible for the effects of senescent cells have not been fully elucidated. Here, we review current knowledge about the beneficial and detrimental effects of senescent cells in tissue repair, regeneration, aging, and age-related disease, especially in skeletal muscle. We also discuss how senescence of muscle stem cells and muscle-resident fibro-adipogenic progenitors affects muscle pathologies or regeneration, and consider the possibility that immunosenescence leads to muscle pathogenesis. Finally, we explore senotherapy, the therapeutic targeting of senescence to treat age-related disease, from the standpoint of improving muscle regeneration.

Impaired aerobic capacity and premature fatigue preceding muscle weakness in the skeletal muscle Tfam-knockout mouse model.

ABSTRACTMitochondrial diseases are genetic disorders that lead to impaired mitochondrial function, resulting in exercise intolerance and muscle weakness. In patients, muscle fatigue due to defects in mitochondrial oxidative capacities commonly precedes muscle weakness. In mice, deletion of the fast-twitch skeletal muscle-specific Tfam gene (Tfam KO) leads to a deficit in respiratory chain activity, severe muscle weakness and early death. Here, we performed a time-course study of mitochondrial and muscular dysfunctions in 11- and 14-week-old Tfam KO mice, i.e. before and when mice are about to enter the terminal stage, respectively. Although force in the unfatigued state was reduced in Tfam KO mice compared to control littermates (wild type) only at 14 weeks, during repeated submaximal contractions fatigue was faster at both ages. During fatiguing stimulation, total phosphocreatine breakdown was larger in Tfam KO muscle than in wild-type muscle at both ages, whereas phosphocreatine consumption was faster only at 14 weeks. In conclusion, the Tfam KO mouse model represents a reliable model of lethal mitochondrial myopathy in which impaired mitochondrial energy production and premature fatigue occur before muscle weakness and early death.

The Assessment of Muscle Mass and Function in Patients with Long-Standing Rheumatoid Arthritis.

Muscular dysfunction in rheumatoid arthritis (RA) can affect the quality of life and comorbidities. We enrolled 320 patients with RA, and evaluated their muscle mass, grip strength, and physical performance. Seven (2.2%) and 21 RA patients (6.6%) had sarcopenia, as defined by the European and Asian Working Group for Sarcopenia (EWGS and AWGS), respectively; 54 patients (16.9%) were determined to have low muscle mass with normal muscle function, as defined by the EWGS; 38 patients (11.9%) reported sarcopenia by SARC-F questionnaire. Male sex (odds ratio (OR) 140.65), low body mass index (BMI) (OR 0.41), and use of tumor necrosis factor (TNF) inhibitors (OR 4.84) were associated with a low muscle mass as defined by the EWGS, while male sex, old age, and low BMI were associated with sarcopenia as defined by the AWGS. Old age (OR 1.11), high BMI (OR 1.13), and a high Disease Activity Score 28 (OR 1.95) were associated with sarcopenia as reported on the SARC-F. Male, low BMI, and use of TNF inhibitors were associated with a low muscle mass, while male sex, old age, and low BMI were associated with sarcopenia in patients with long-standing RA.