This paper evaluates severe normal trunk asymmetry (TA) by higher and lower body mass index (BMI) values in 5953 adolescents age 11–17 years (boys 2939, girls 3014) whilst standing forward bending (FB) and sitting FB during screening for scoliosis. TA was measured as angle of trunk inclinations (ATIs) across the back (thoracic, thoracolumbar and lumbar) with abnormality defined as 2 standard deviations or more. The findings for sitting FB position are reported because the readings express TA free from any leg-length inequality. Relatively lower BMIs are associated statistically with. excess of abnormal TAs, and. later menarche. BMI is known to be linked to puberty timing and energy balance but not to TAs in healthy students. Similar to girls with adolescent idiopathic scoliosis, we suggest that severe TA is caused by a genetically-determined selectively increased hypothalamic sensitivity to leptin with asymmetry as an adverse hormetic response, exacerbated by presumed lower circulating leptin levels associated with relatively lower BMIs. The asymmetry is expressed bilaterally via the sympathetic nervous system to produce left-right asymmetry in ribs and/or vertebrae leading to severe TA when beyond the capacity of postural mechanisms of the somatic nervous system to control the shape distortion of the trunk

Osteoarthritis (OA) is a highly prevalent degenerative joint disorder characterized by joint pain and physical disability. Aberrant subchondral bone induces pathological changes and is a major source of pain in OA. In the subchondral bone, which is highly innervated, nerves have dual roles in pain sensation and bone homeostasis regulation. The interaction between peripheral nerves and target cells in the subchondral bone, and the interplay between the sensory and sympathetic nervous systems, allow peripheral nerves to regulate subchondral bone homeostasis. Alterations in peripheral innervation and local transmitters are closely related to changes in nociception and subchondral bone homeostasis, and affect the progression of OA. Recent literature has substantially expanded our understanding of the physiological and pathological distribution and function of specific subtypes of neurones in bone. This review summarizes the types and distribution of nerves detected in the tibial subchondral bone, their cellular and molecular interactions with bone cells that regulate subchondral bone homeostasis, and their role in OA pain. A comprehensive understanding and further investigation of the functions of peripheral innervation in the subchondral bone will help to develop novel therapeutic approaches to effectively prevent OA, and alleviate OA pain. Cite this article: Bone Joint Res 2022;11(7):439–452

Objectives. In order to elucidate the influence of sympathetic nerves on lumbar radiculopathy, we investigated whether sympathectomy attenuated pain behaviour and altered the electrical properties of the dorsal root ganglion (DRG) neurons in a rat model of lumbar root constriction. Methods. Sprague-Dawley rats were divided into three experimental groups. In the root constriction group, the left L5 spinal nerve root was ligated proximal to the DRG as a lumbar radiculopathy model. In the root constriction + sympathectomy group, sympathectomy was performed after the root constriction procedure. In the control group, no procedures were performed. In order to evaluate the pain relief effect of sympathectomy, behavioural analysis using mechanical and thermal stimulation was performed. In order to evaluate the excitability of the DRG neurons, we recorded action potentials of the isolated single DRG neuron by the whole-cell patch-clamp method. Results. In behavioural analysis, sympathectomy attenuated the mechanical allodynia and thermal hyperalgesia caused by lumbar root constriction. In electrophysiological analysis, single isolated DRG neurons with root constriction exhibited lower threshold current, more depolarised resting membrane potential, prolonged action potential duration, and more depolarisation frequency. These hyperexcitable alterations caused by root constriction were significantly attenuated in rats treated with surgical sympathectomy. Conclusion. The present results suggest that sympathectomy attenuates lumbar radicular pain resulting from root constriction by altering the electrical property of the DRG neuron itself. Thus, the sympathetic nervous system was closely associated with lumbar radicular pain, and suppressing the activity of the sympathetic nervous system may therefore lead to pain relief

A rat model of lumbar root constriction with an additional sympathectomy in some animals was used to assess whether the sympathetic nerves influenced radicular pain. Behavioural tests were undertaken before and after the operation. On the 28th post-operative day, both dorsal root ganglia and the spinal roots of L4 and L5 were removed, frozen and sectioned on a cryostat (8 μm to 10 μm). Immunostaining was then performed with antibodies to tyrosine hydroxylase (TH) according to the Avidin Biotin Complex method. In order to quantify the presence of sympathetic nerve fibres, we counted TH-immunoreactive fibres in the dorsal root ganglia using a light microscope equipped with a micrometer graticule (10 x 10 squares, 500 mm x 500 mm). We counted the squares of the graticule which contained TH-immunoreactive fibres for each of five randomly-selected sections of the dorsal root ganglia. The root constriction group showed mechanical allodynia and thermal hyperalgesia. In this group, TH-immunoreactive fibres were abundant in the ipsilateral dorsal root ganglia at L5 and L4 compared with the opposite side. In the sympathectomy group, mechanical hypersensitivity was attenuated significantly. We consider that the sympathetic nervous system plays an important role in the generation of radicular pain

Osteoarthritis (OA) affects the whole joint and leads to chronic pain. The sympathetic nervous system (SNS) seems to be involved in OA pathogenesis, as indicated by in vitro studies as well as by our latest work demonstrating that sympathectomy in mice results in increased subchondral bone volume in the OA knee joint. We assume that chronic stress may lead to opposite effects, such as an increased bone loss in OA due to an elevated sympathetic tone. Therefore, we analyzed experimental OA progression in mice exposed to chronic stress. OA was induced in male C57BL/6J mice by surgical destabilization of the medial meniscus (DMM) and Sham as well as non-operated mice served as controls. Half of these groups were exposed to chronic unpredictable mild stress (CUMS). After 12 weeks, chronic stress efficiency was assessed using behavioral tests. In addition to measuring body weight and length, changes in subchondral bone were analyzed by μCT. Dynamic Weight Bearing system was used to monitor OA-related pain. Histological scoring will be conducted to investigate the severity cartilage degeneration and synovial inflammation. CUMS resulted in increased anxiety and significant decrease in body weight gain in all CUMS groups compared to non-CUMS groups. CUMS also increased serum corticosterone in healthy mice, with even higher levels in CUMS mice after DMM surgery. CUMS had no significant effect on subchondral bone, but subarticular bone mineral density and trabecular thickness were increased. Moreover, CUMS resulted in significant potentiation of DMM-associated pain. Our results suggest that the autonomic imbalance with increased sympathetic nervous activity induced by chronic stress exacerbates the severity of OA pain perception. We expect significantly increased cartilage degeneration as well as more severe synovial inflammation in CUMS DMM mice compared to DMM mice

Introduction. Osteoarthritis (OA) is a chronic degenerative disease of the entire joint leading to joint stiffness and pain (PMID:33571663). Recent evidence suggests that the sympathetic nervous system (SNS) plays a role in the pathogenesis of OA (PMID:34864169). A typical cause for long-term hyperactivity of the SNS is chronic stress. To study the contribution of increased sympathetic activity, we analyzed the progression of OA in chronically stressed mice. Method. We induced OA in male C57BL/6J mice by destabilizing the medial meniscus (DMM)(PMID:17470400) and exposed half of these mice to chronic unpredictable mild stress (CUMS)(PMID:28808696). Control groups consisted of sham-operated mice with and without CUMS exposure. After 12 weeks, CUMS efficacy was determined by assessing changes in body weight gain and activity of mice, measuring splenic norepinephrine and serum corticosterone levels. OA progression was studied by histological analysis of cartilage degeneration and synovitis, and by μCT to evaluate changes in calcified cartilage and subchondral bone microarchitecture. A dynamic weight-bearing system was used to assess OA-related pain. Result. CUMS resulted in significantly decreased body weight gain and activity, as well as increased splenic norepinephrine and serum corticosterone concentrations compared to the respective controls. Surprisingly, already DMM alone resulted in elevated stress hormone levels. CUMS significantly exacerbated cartilage degeneration and synovial inflammation and increased OA pain in DMM mice. The underlying cellular and molecular mechanisms are currently being analyzed using FACS, single cell RNAseq, and spatial proteomics. Conclusion. Overall, chronic stress exacerbates OA severity and pain. Moreover, increased levels of stress hormones were observed in OA mice without CUMS induction, suggesting a complex bi-directional interaction between the SNS and OA. Targeting the autonomic nervous system, such as attenuating the SNS but also stimulating the activity of the parasympathetic nervous system, as a counterpart of the SNS, may therefore be promising for novel preventive or causal treatments of OA

Purpose and Background: Physiotherapeutic management of lumbar disorders often incorporates specific manual therapy techniques of which McKenzie’s lumbar extension exercises (EIL) and segmental rotational grade V manipulation are popular options. The use of proxy measures of sympathetic nervous system (SNS) activity (skin conductance) is a recognised method of ascertaining neurophysiological responses to physiotherapy treatment but have yet to be used to assess magnitude of response to lumbar techniques. This preliminary study aimed to investigate the neurophysiological effects of these two treatment techniques. Methodology: A quasi-experimental, independent group’s design was utilised, with random allocation of 50 normal, healthy participants (25 per group) into a manipulation group or an EIL group. Non-invasive neurophysiological measurements of skin conductance were taken as a proxy-measure of sympathetic nervous system (SNS) activity in the lower limbs before, during and after the administration of the techniques. Results were calculated using Area Under the Curve readings and converted into percentage change calculations for the intervention and the post-intervention periods. Results: Both treatments increased SNS activity during the intervention period, 76% for the manipulation group (p=0.0005) and 35% for EIL group (p=0.0005) with the manipulative technique having significantly greater effect (p=0.012). Further analysis of the manipulation group found no difference between the ‘opening’ and the ‘closing’ side of the technique (p=0.76). Conclusion: Preliminary evidence now exists supporting the neurophysiological effects of two lumbar techniques and that manipulation has a greater magnitude of effect over the EIL technique. Future research, on a low back pain patient population, is proposed and projected sample size calculations computed

Introduction. In patients with adolescent idiopathic scoliosis (AIS), anomalous extra-spinal left-right skeletal length asymmetries in upper limbs, periapical ribs, and ilia beg the question as to whether these bilateral asymmetries are connected in some way with pathogenesis. The upper arm and iliac length asymmetries correlate significantly with adjacent spinal curve severity respectively in thoracic and lower (thoracolumbar and lumbar) spine. In lower limbs, skeletal length asymmetries and proximo-distal disproportion are unrelated to spinal curve severity. Overall, these observations raise questions about mechanisms that determine skeletal bilateral symmetry of vertebrates in health and disorder, and whether such mechanisms are involved in the cause of this disease. We investigated upper arm length (UAL) asymmetries in two groups of right-handed girls aged 11–18 years, with right thoracic adolescent idiopathic scoliosis (RT-AIS, n=98) from preoperative and screening referrals (mean Cobb angle 45°) and healthy controls (n=240). Methods. Right and left UAL were measured with a Harpenden anthropometer of the Holtain equipment, by one of four observers (RGB, AAC, RKP, FJP). UAL asymmetry was calculated as UAL difference, right minus left, in mm. Repeatability of the measurements was assessed by technical error of the measurement (TEM) and coefficient of reliability (R). Results. In girls with RT-AIS, UAL asymmetry was greater than it was in healthy girls (mean 5·9 mm vs 2·5 mm, ANOVA p<0·001, correcting for age), regressed negatively with age (p<0·001, r= –0·374), and correlated significantly with Cobb angle (r=0·342, p=0·001) and apical vertebral rotation (Perdriolle, r=0·291, p=0·004). In healthy girls, UAL asymmetry was unrelated to age. Plotted against years after estimated menarcheal age, right UAL overgrowth reduced significantly for girls with RT-AIS (r= –0·312, p=0·006, n=76) but not for healthy girls (r=0·000, p=0·985, n=121), which was a significant finding (p=0·052, ANOVA). Conclusions. The abnormal overgrowth of right upper arm length may be secondary, or pathogenetically associated with the RT-AIS trunk deformity. The negative regression of UAL asymmetry may result from (1) older girls having less residual growth and/or (2) a transient, or resolving, asymmetry process common to arm and trunk. We hypothesise that the pathogenetic process of RT-AIS may include two components: a transient bilateral asymmetry process and growth velocity, both of which affect trunk and arm growth. In the spine, these rarely lead to scoliosis resolution because biomechanical, postural, melatonin-signalling, and other factors sustain and aggravate the curve. Four pathomechanisms may induce the asymmetry process in trunk and arms involving (1) neuromuscular function, (2) motor cortex, (3) sympathetic nervous system, and (4) intrinsic time-tallies in growth plates, some of which suggest therapeutic possibilities

Aims

Rotator cuff muscle atrophy and fatty infiltration affect the clinical outcomes of rotator cuff tear patients. However, there is no effective treatment for fatty infiltration at this time. High-intensity interval training (HIIT) helps to activate beige adipose tissue. The goal of this study was to test the role of HIIT in improving muscle quality in a rotator cuff tear model via the β3 adrenergic receptor (β3AR).

Objectives

Many in vitro studies have investigated the mechanism by which mechanical signals are transduced into biological signals that regulate bone homeostasis via periodontal ligament fibroblasts during orthodontic treatment, but the results have not been systematically reviewed. This review aims to do this, considering the parameters of various in vitro mechanical loading approaches and their effects on osteogenic and osteoclastogenic properties of periodontal ligament fibroblasts.

The stress response to trauma is the summation of the physiological response to the injury (the ‘first hit’) and by the response to any on-going physiological disturbance or subsequent trauma surgery (the ‘second hit’).

Our animal model was developed in order to allow the study of each of these components of the stress response to major trauma. High-energy, comminuted fracture of the long bones and severe soft-tissue injuries in this model resulted in a significant tropotropic (depressor) cardiovascular response, transcardiac embolism of medullary contents and activation of the coagulation system. Subsequent stabilisation of the fractures using intramedullary nails did not significantly exacerbate any of these responses.

Complex regional pain syndrome is characterised by an exaggerated response to injury in a limb with intense prolonged pain, vasomotor disturbance, delayed functional recovery and trophic changes. This review describes the current knowledge of the condition and outlines the methods of treatment available with particular emphasis on the knee.