Success treating AIS with bracing is related to time worn and scoliosis severity. Temperature monitoring can help patients comply with their orthotic prescription. Routinely collected temperature data from the start of first brace treatment was reviewed for 14 patients. All were female with an average age of 12.4 years (range 10.3–14.6) and average 49o Cobb angle (30–64). Our current service recommendation is brace wear for 20 hours a day. Patients complied with this prescription 38.0% of the time, with four patients averaging this or more. Average brace wear was 16.3 hours per day (3.5–22.2). There were 13 patients who had completed brace treatment. The majority had surgery (7/13; 54%) or were considering surgery (1/13; 8%). There were 5 who did not wish surgery at discharge (5/13; 38%); 1 achieved a 40o Cobb angle, with 4 larger (53o;53o;54o;68o). The Bracing in AIS Trial (BrAIST) study measured “success” as less than a 50o Cobb angle, so using this metric our cohort has had a single “success”. Temperature monitors allowed an analysis of when patients were achieving their brace wear. When comparing daywear (8am-8pm) to nightwear (8pm-8am), patients wore their brace an average of 7.6 hours a day (2.5–11.2) and 8.7 hours a night (0.4–11.5). We conclude the minority of our patients comply with our current 20 hour orthotic prescription. The “success” of brace treatment is lower than comparison studies despite higher average compliance but starting with a larger scoliosis. Brace wear is achieved during both the day and night.
Single shot interscalene blocks are an effective analgesic for arthroscopic shoulder surgery. However, patients receiving these blocks are often found to be in significant pain when the block wears off, usually in the late evening or early hours of the morning. Overnight admission is currently routine in our unit, to ensure adequate analgesia can be administered during this period. Recent studies have suggested that adding dexamethasone to the local anaesthetic agent can prolong the duration of the block. We carried out a prospective study to assess whether addition of dexamethasone to brachial plexus blocks could reduce patient's post-operative analgesic demands and allow safe discharge on the same day after surgery. Twenty-six patients undergoing arthroscopic shoulder surgery during a morning theatre list, had ultrasound guided brachial plexus blocks using a mixture of 0.25% bupivacaine 20–30ml with 2–3mg of dexamethasone. All were admitted to the ward afterwards for analgesia and physiotherapy. Pain numerical rating scores (0–10) were recorded at rest in recovery one hour postoperatively by the attending anaesthetist and on active movement of the shoulder joint 24 hours after surgery by the attending physiotherapist. A standardised analgesia regime was prescribed with regular and as required medication, including as required strong opiates. Mean pain scores in recovery were 0.31 and on the morning after surgery were 2.38. Sixteen out of 26 required no further analgesia, with only 3 out of the 10 who did requiring opiates. The use of dexamethasone provides adequate analgesia for a prolonged period for most patients after brachial plexus block for shoulder surgery and does not result in a significant analgesic requirement when the block wears off. This may provide support for avoiding overnight admission in selected patients after arthroscopic shoulder surgery.
Six week old male Sprague-Dawley rats were administered intravenous clozapine, quetiapine, haloperidol or vehicle once daily for a period of 42 days with access to only high fat diet and their weight was monitored regularly. At the end of the study the rats were killed and the tibiae excised and bone mineral density (BMD) measured with dual X-ray absorptiometry and bone architecture assessed with micro-computed tomography (micro-CT) and associated software. Results were subjected to one-way ANOVA and post hoc Dunnetts multiple comparison test. All treatment groups were compared to control. There were no significant differences in body weight between the different groups at completion of the study. Clozapine treated animals alone showed a significant reduction in bone mineral density (p<0.05) however no differences were seen with haloperidol and quetiapine. Both haloperidol and quetiapine, but not clozapine, treatment showed a significant reduction in the bone to tissue volume ratio (BV/TV) by approximately 23% (p<0.05) and an increase in trabecular number (TbN) by approximately 21% (p<0.05). Trabecular bone architecture parameters for haloperidol and quetiapine, but not clozapine, showed more rod like and disconnected structure as reflected in the increases in structure model index (SMI) of around 15% (p<0.05) and trabecular pattern factor (TbPf) by 22% (p<0.05). This data demonstrates that in rats receiving a high fat diet, haloperidol and quetiapine have an adverse effect on bone micro-architecture without significant change in whole body bone mineral density. Clozapine did not affect bony architecture in a significant manner as reported in our earlier study, though bone mineral density was reduced. Reasons for the different effect of clozapine in this study are still uncertain but may be related to the significant weight loss seen at the end point of the previous study. Causes for osteoporosis and increased fracture risk in schizophrenia may include smoking history, malnutrition, limited sun exposure and compliance. Long term administration of both typical and atypical anti-psychotics may have a negative effect on bone and is a further factor that can influence this risk. An awareness of this relationship is useful in the orthopaedic management of schizophrenic patients.
Delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) permits inference of glycosaminoglycan (GAG) distribution. We aimed to determine whether hips with cam deformities have altered GAG content, using dGEMRIC.
2 regions of interest (ROI) were studied:
acetabular cartilage from 12 to 3 O’Clock (T1-Index-acet). total cartilage (femoral and acetabular) for the joint from 9 to 3 O’Clock (T1-Indextotal). The average of all pixels within the given ROI defined the T1-index. For each hip, the ratio of the GAG content T1-Index-acet/T1-Indextotal was calculated. Mean T1-Indexto-tal and T1-Indexacet/T1-Indextotal were compared.
Leptin is a major hormonal product of the adipocyte which regulates appetite and reproductive function through its hypothalamic receptors. It has now become clear that leptin receptors are much more widely distributed than just the hypothalamus, and the skeleton has emerged as an important site of action of leptin. The signalling form of the leptin receptor has been found in several cell types including human osteoblasts, rat osteoblasts and human chondrocytes. In vitro we have shown leptin to an anabolic factor, stimulating osteoblast proliferation and inhibiting osteoclastogenesis. Leptin increases bone mass and reduces bone fragility when administered peripherally but has an indirect inhibitory effect on bone mass via the hypothalamus when administered directly into the central nervous system. Data from animal models where there is an absence of either leptin production (ob/ob) or its receptor (db/db) have been contradictory. In this study we compared the bone phenotype of leptin receptor-deficient (db/db) and wild-type (WT) mice. Micro-CT analysis was done on proximal tibiae using a Skyscan 1172 scanner. Db/db mice had significantly reduced trabecular bone volume, trabecular thickness and trabecular number and a higher degree of trabecular separation. Cortical bone was also significantly lower in db/db animals in volume, cross-sectional thickness and perimeter. These results demonstrate that in the absence of leptin signalling there is reduced bone mass indicating that leptin indeed acts in vivo as a bone anabolic factor, mimicking the in vitro results.
Adiponectin, a hormone secreted by adipocytes, regulates energy homeostasis and glucose and lipid metabolism. Plasma levels of adiponectin are negatively correlated with body fat mass. Adiponectin inhibits the formation and activity of osteoclasts and increases the proliferation and differentiation of osteoblasts in vitro. The aim of our study was to determine the bone phenotype of adiponectin knockout mice. Male adiponectin-deficient (Ad-KO) and wild-type (WT) C57BL/6J mice were sacrificed at 8, 14 and 22 weeks of age. Body weights did not differ between Ad-KO and WT mice. We scanned the left proximal tibia using micro-CT at 5μm resolution and analysed bone microarchitecture by 3D analysis. We found significant increases in trabecular bone volume (BV/TV) (15.9±1.63 vs. 12.2±0.72%, p=0.02) and trabecular number (3.20±0.18mm-1 vs. 2.32±0.12mm-1, p=0.0009) in 14-week old Ad-KO mice compared to controls. Similar differences between WT and Ad-KO were present in 8 and 22-week old animals but these did not reach statistical significance. Trabecular thickness was significantly greater (0.053±0.001mm vs. 0.048±0.002mm, p=0.04) in 22-week old Ad-KO mice compared to WT. Ad-KO mice have increased number and volume of trabeculae at 14 weeks of age indicating that the net effect of adiponectin on bone accrual in vivo is inhibitory. These effects are age-dependent. Our data concur with the observations from epidemiological studies in humans that adiponectin negatively correlates with both fat mass and bone mass. Therefore, adiponectin may be a contributor to the link between fat and bone mass.