Patients living with type 1 diabetes mellitus (T1DM) can develop early onset osteoporosis and are exposed to an increased risk of fracture. Skeletal health can be influenced easily with diet and exercise. However, diabetes mellitus (DM)-related osteopathy is not emphasized in the public information campaigns on the American Diabetes Association, Diabetes UK, Diabetes Ireland or International Diabetes Federation websites. This investigation aims to assess the perceptions of patients regarding living with T1DM and their baseline knowledge on DM-related osteopathy. A survey was administered to 102 consenting individuals living with T1DM in attendance at the Galway University Hospital Diabetes Centre. Of the respondents, 44% were female and 56% male (mean age of 43). Respondents had T1DM for a mean of 21 years. Participants were asked to identify DM-related complications, including bone thinning and bone fractures. Respondents were primarily concerned about developing DM-related blindness, kidney damage and amputations, but not osteopathy. 49% of respondents did not identify osteopathy as a potential DM-related complication, 28% of respondents related DM with bone thinning and bone fractures, and 22% individuals only identified bone thinning or bone fractures. When asked for their primary source of DM-related information, endocrinologists and internet where identified. When comparable questions were asked of DM-related healthcare professionals, 56% did not recognize osteopathy as a complication of T1DM. This study demonstrated a low-level awareness of the impact living with T1DM has on bone health. The deployment of patient-interactive activities or educational modules may enhance the future health of individuals living with T1DM

Introduction and Objective. Type 2 diabetes mellitus (T2DM), and the often concurrent obesity, causes metabolic changes that affect many organs and tissues, including bone. Despite a normal or even higher bone mineral density (BMD), T2DM has often been associated with a higher fracture risk, indicating a compromised bone quality. In this work, we use a novel congenic leptin receptor-deficient BioBreeding Diabetes Resistant rat (BBDR.cg.lepr.cp) to investigate the impact of T2DM and obesity on bone morphology and architecture at the microscale. Materials and Methods. Two different anatomical locations, i.e., femur and cranium, were studied combining micro-computed X-ray tomography (micro-CT) with scanning electron microscopy (SEM). Micro-CT data were examined using advanced image analysis tools in three-dimensions (3D). Results. Both parietal bones and femurs were smaller, i.e., thinner and shorter, respectively, in diabetic animals compared to healthy controls. Image analysis of the sagittal suture revealed a reduced suture width and length in diabetic animals, suggesting an altered bone apposition rate. Histomorphometry analysis from micro-CT data highlighted differences in microstructure of both trabecular and cortical femur between diabetic and healthy rats. In particular, bone volume fraction (BV/TV) was lower in the T2DM group, while trabecular spacing (Tb.Sp) was increased, overall indicating a higher porosity in diabetic trabecular bone. SEM revealed the presence of extended portions of hyper-mineralized cartilage in the distal femur of the diabetic animals. Conclusions. Micro-CT analyses, combined with SEM imaging, suggest that T2DM impacts bone growth and remodelling, in turn leading to differences in the structural organization at the microscale

Abstract. Objectives. Diabetes has been associated with greater risk of complications and prolonged postoperative recovery following ankle trauma. Our cohort study seeks to review the operative management and outcomes of ankle fractures in diabetic adults relative to non-diabetic adults. Methods. Cases were identified using ICD-10 coding criteria. 572 patients from Jan 2016–2019 presented with ankle fractures; 34 in diabetic patients. Mechanism of injury and stability were determined from the index radiograph using a validated Lauge-Hansen classification algorithm. Admission, primary post-operative and discharge radiographs were reviewed independently by two foot and ankle reconstruction specialists to assess adequacy of fixation method. 32% of diabetic patients were managed non-operatively compared to 29% of the matched non-diabetic cohort. The distribution in Lauge-Hansen fracture pattern was comparable between cohorts. Non-diabetic controls were frequency age-matched 2:1. Results. Mean length of follow-up was significantly longer for diabetics (26 weeks) compared to non-diabetics (16 weeks). Post-operative wound complications (superficial wound infection, breakdown, dehiscence) occurred in 48% of the operated diabetic ankles, compared to 5% in non-diabetics (RR 8.1, 95% CI 2.5–26.4). Reoperation (RR 4.3, 95% CI 2.5–26.4, p=0.03) and non-wound complication rates (Charcot joint, mal/non-union, metalwork infection) were likewise significantly higher (RR 3.9, 95% CI 1.4–10.8, p=0.008) in diabetics. Amongst diabetics alone, those with an HbA1c >69 mmol/mol (n=14, 41%) demonstrated a significantly higher rate still of non-wound complications (RR 4.3, 95% CI 1.1–18., p=0.03) with a trend towards higher wound complication rates (RR 3, 95% CI 0.52–17, p=0.13). Conclusions. Poorly controlled diabetes is associated with substantially greater complication rates following ankle fracture than those with well controlled or normal blood sugar; high HbA1c > 69mmol/mol is a significant predictor of complicated follow-up. Locally we recommend management strategies that are influenced by the fracture pattern stability and the presence or absence of complicated or poorly managed diabetes. Declaration of Interest. (b) declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported:I declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project

Diabetes has been associated with greater risk of complications and prolonged postoperative recovery following ankle trauma. Our cohort study reviewed the operative management and outcomes of ankle fractures in diabetic adults relative to non-diabetic adults from Jan 2016–2019. Non-diabetic controls were frequency age-matched 2:1. 34 of 572 ankle fracture presentations were in diabetic patients, 32% managed non-operatively compared to 29% of the matched non-diabetic cohort. The distribution in Lauge-Hansen fracture pattern was comparable between cohorts. Mean length of follow-up was significantly longer for diabetics (26 weeks) compared to non-diabetics (16 weeks). Post-operative wound complications (superficial wound infection, breakdown, dehiscence) occurred in 48% of the operated diabetic ankles, compared to 5% in non-diabetics (RR 8.1, 95% CI 2.5–26.4). Reoperation (RR 4.3, 95% CI 2.5–26.4, p=0.03) and non-wound complication rates (Charcot joint, mal/non-union, metalware infection) were likewise significantly higher (RR 3.9, 95% CI 1.4–10.8, p=0.008) in diabetics. Amongst diabetics alone, those with an HbA1c >69 mmol/mol (n=14, 41%) demonstrated a significantly higher rate still of non-wound complications (RR 4.3, 95% CI 1.1–18., p=0.03) with a trend towards higher wound complication rates (RR 3, 95% CI 0.52–17, p=0.13). Poorly controlled diabetes is associated with substantially greater complication rates following ankle fracture than those with well controlled or normal blood sugar; high HbA1c > 69mmol/mol is a significant predictor of complicated follow-up. Locally we recommend management strategies that are influenced by the fracture pattern stability and the presence or absence of complicated or poorly managed diabetes

Fragility fractures are skeletal complications associated with type 2 diabetes (T2D) causing disability, hospitalization, impaired quality of life, and increased mortality. Increased circulating sclerostin and accumulation of advanced glycation end-products (AGEs) are two potential mechanisms underlying low bone turnover and increased fracture risk. We have recently shown that T2D affects the expression of genes controlling bone formation (SOST and RUNX2) and that accumulation of AGEs is associated with impaired bone formation in T2D. We hypothesized that Wnt/B- catenin target genes are down-regulated in bone of T2D subjects as a consequence of decreased SOST and AGEs accumulation. To this end, we studied gene expression in extracts of bone samples obtained from femoral heads of 14 subjects with relatively well-controlled T2D (HbA1c 6.5±1.7%) and 21 control, non-diabetic postmenopausal women (age >65 years) undergoing hip replacement. There were no differences in age (73.2± .8 vs. 75.2±8.5 years) or BMI (27.7±5.6 vs. 29.9±5.4 kg/m2) between control and T2D groups, respectively. Expression of LEF1 mRNA was significantly lower in T2D compared to non-diabetic subjects (p=0.002), while DKK1 was not different between groups (p=0.108). Correlation analysis showed that DKK1 (r2=0.038; p=0.043) and HbA1c (r2=0.503; p=0.048) increased with age in T2D. COL1A1 mRNA trended lower in T2D compared to controls (p=0.056). Bone volume (9,333 ± 1,443 vs. 15,53 ± 2,442 mm2; p=0.048), mineralized volume (9,278 ± 1,418 vs. 15,45 ± 2,444 mm. 2. ; p=0.048) and BV/TV (0,2125 ± 0,03114 vs. 0,3719 ± 0,03196 %; p=0.002) measured by bone histomorphometry were lower in T2D compared to controls. Our data show that even in patients with relatively good glycemic control, T2D decreases expression of Wnt/B-catenin target genes andCOL1A1, associated with decreased bone density. These results may help understand the mechanisms underlying bone fragility in T2D

Introduction. Tendon disease and rupture are common in patients with diabetes and these are exacerbated by poor healing. although nanoscale changes in diabetic tendon are linked to increased strength and stiffness. The resistance to mechanical damage of a tissue may be measured using fatigue testing but this has not been carried out in diabetic tendon, although the toughness of diabetic bone is known to be reduced. The aim of this study was to measure the static fatigue behaviour of tendons from a streptozotocin (STZ)-induced rat model of diabetes, hypothesising that diabetes causes tendon to show lower resistance to mechanical damage than healthy tendon. Materials and Methods. Diabetic (n=3, 12 weeks post-STZ) and age-matched control (n=3) adult male Sprague Dawley rats were culled, tails harvested and stored at −80ºC. Following defrosting, fascicles (5 per animal) were carefully dissected, mean diameter measured using an optical micrometer and mounted in a Bose Biodynamics test machine using custom grips in a PBS bath. Static fatigue testing at 30 MPa to failure enabled both elastic modulus (initial ramp) and steady state creep rate (gradient at creep curve inflexion) to be measured. Data are reported as median ± interquartile range and pw0.05 using a Mann-Whitney U test was taken as significant. Results. Confirming previous reports, tendon from diabetic rats showed significantly higher elastic modulus (201 ± 68 MPa) than healthy (151 ± 62 MPa). Strain at failure showed no differences between groups. Tendon from diabetic rats showed significantly slower steady state creep (71 ± 44 μstrain s. −1. ) than healthy (691 ± 1000 μstrain s. −1. ). Discussion. These preliminary data show an order of magnitude larger resistance to mechanical damage in diabetic tendons, possibly associated with the previously reported increased packing and decreased fibril diameters. Energy-storing flexor tendons, the most commonly affected in diabetics, and the positional tendons tested here show similar fatigue behaviour when tested at the same fraction of “stress-in-life”. Further investigation is required into the cell tissue repair response in diabetes in order to link reduced rates of mechanical damage with the clinically increased risk of disease and rupture in diabetic patients

Intervertebral disc degeneration (IDD) is a major cause of low back pain, which affects 80% of the adult population at least once in their life. The pathophysiological conditions underlying IDD are still poorly understood. Genetic makeup, aging, smoking, physical inactivity and mechanical overloading, especially due to obesity, are among the strongest risk factors involved. Moreover, IDD is often associated with chronic inflammation within disc tissues, which increases matrix breakdown, glycosaminoglycan (GAG) loss and cell death. This micro-inflammatory environment is typical of several metabolic disorders, including diabetes mellitus (DM). As the etiopathogenesis of IDD in diabetic subjects remains scarcely understood, we hypothesised that this may be driven by a DM-induced inflammation leading to a combination of reduced GAG levels, decreased proteoglycan synthesis and increased matrix breakdown within the disc. The objective of the study was to investigate the pathogenesis of IDD in a murine model of type 1 DM (T1DM), namely non-obese diabetic (NOD) mouse. Total disc glycosaminoglycan (GAG) content, proteoglycan synthesis, aggrecan fragmentation mediated by matrix metalloproteinases (MMPs) and a Disintegrin and Metalloproteinase with Thrombospondin motifs (ADAMTS), glucose transporter (mGLUT1) gene expression and apoptosis (TUNEL assay) were assessed in NOD mice and wild-type euglycemic control mice. Spinal structural and molecular changes were analysed by micro-computed tomography (mCT), histological staining (Safranin-O and fast green) and quantitative immunofluorescence (anti-ADAMTS-4 and 5 antibodies). Statistical analysis was conducted considering the average of 35 samples ± standard error for each measurement, with 95% confidence intervals calculated to determine statistical significance (p-value < 0.05). IVDs of NOD mice showed increased disc apoptosis (p < 0.05) and higher aggrecan fragmentation mediated by ADAMTS (p < 0.05). However, ADAMTS-4 and −5 did not appear to be involved in this process. The total GAG content normalized to DNA and PG synthesis showed no statistically significant alterations, as well as Safranin O staining. Although not significantly, NOD mice showed reduced glucose uptake. In addition, the vertebral structure of NOD mice at mCT seemed not to be altered. These data demonstrate that DM may contribute to IDD by increasing aggrecan degradation and promoting cell apoptosis, which may represent early indicators of the involvement of DM in the pathogenesis of IDD

An international Consensus Group has by a Delphi approach identified the topic of host factors affecting pin site infection to be one of the top 10 priorities in external fixator management. The aim of this study was to report the frequency of studies reporting on specific host factors as a significant association with pin site infection. Host factors to be assessed was: age, smoking, BMI and any comorbidity, diabetes, in particular. The intention was an ethological review, data was extracted if feasible, however no meta-analysis was performed. A systematic literature search was performed according to the PRISMA-guidelines. The protocol was registered before data extraction in PROSPERO. The search string was based on the PICO criterias. A logic grid with key concept and index terms was made. A search string was built assisted by a librarian. The literature search was executed in three electronic bibliographic databases, including Embase MEDLINE (1111 hits) and CINAHL (2066 hits) via Ovid and Cochrane Library CENTRAL (387 hits). Inclusion criteria: external fixation, >1 pin site infection, host factor of interest, peer-reviewed journal. Exclusion criteria: Not written in English, German, Danish, Swedish, or Norwegian, animal or cadaveric studies, location on head, neck, spine, cranium or thorax, editorials or conference abstract. The screening process was done using Covidence. A total of 3564 titles found. 3162 excluded by title and abstract screening. 140 assessed for full text eligibility. 11 studies included for data extraction. The included studies all had a retrospective design. Three identified as case-control studies. Generally the included studies was assessed to have a high risk of bias. A significant associations between pin site infection for following host factors: a) increased HbA1C level in diabetic patients; b) congestive heart failure in diabetic patients; c) less co-morbidity; d) preoperative osteomyelitis was found individually. This systematic literature search identified a surprisingly low number of studies examining for risk of pin site infection and host factors. Thus, this review most of all serves to demonstrate a gap of evidence about correlation between host factors and risk of pin site infection, and further studies are warranted

The international literature base demonstrates that individuals living with diabetes mellitus (DM) are at increased risk of mortality and post-operative complications following hip fracture surgery (HFS) than non-diabetics. Studies investigating databases in American, European or Asiatic populations highlight the impact geography can have on the resultant investigation. We aim to quantify the impact DM has on HFS patients in a single university hospital. The HIPE dataset of fragility fractures occurring in Galway University Hospital from 2014–2016 were analysed and cross referenced with hospital laboratory and public databases. A database of 759 individuals was created including 515 females and 237 males, with a mean age of 78+/−12.2 years, of which 110 patients had DM. The patient length-of-stay (PLOS) was comparable in all groups with patient age being the primary influencing factor. An extended PLOS correlated with an increased long-term mortality. A trend toward increased occurrence of sub-trochanteric fractures was observed in diabetics with fewer periprosthetic and intertrochanteric fractures. Patients with DM had a significant increased risk of post-operative mortality compared to non-diabetics. Males with DM where at a greater risk of death after HFS [HR 2.29, 95% CI 1.26–4.17. p=0.006] than females with DM [HR 1.69, 95% CI 0.99–2.91. p=0.056]. The presence of DM did not directly impact a patient's PLOS or increase the need for a re-operation. DM is associated with increased post-operative patient mortality and may influence the anatomical fracture pattern. This observation will support further investigation into the mechanical and biochemical changes occurring in the femur in individuals living with DM

Type-2 Diabetic (T2D) patients experience up to a 3-fold increase in bone fracture risk[1]. Paradoxically, T2D-patients have a normal or increased bone mineral density when compared to non-diabetic patients. This implies that T2D has a deleterious effect on bone quality, whereby the intrinsic material properties of the bone matrix are altered. Creating clinical challenges as current diagnostic techniques are unable to accurately predict the fracture probability in T2D-patients. To date, the relationship between cyclic fatigue loading, mechanical properties and microdamage accumulation of T2D-bone tissue has not yet been examined and thus our objective is to investigate this relationship.

Ethically approved femoral heads were obtained from patients, with (n=8) and without (n=8) T2D. To obtain the mechanical properties of the sample, one core underwent a monotonic compression test to 10% strain, the other core underwent a cyclic compression test at a normalized stress ratio between 0.0035mm/mm and 0.016mm/mm to a maximum strain of 3%. Microdamage was evaluated by staining the tissue with barium sulfate precipitate [2] and conducting microcomputed tomography scanning with a voxel size of 10μm.

The monotonically tested T2D-group showed no statistical difference in mechanical properties to the non-T2D-group, even when normalised against BV/TV. There was also no difference in BV/TV. For the cyclic test, the T2D-group had a significantly higher initial modulus (p<0.01) and final modulus (p<0.05). There was no difference in microdamage accumulation.

Previous population-level studies have found that T2D-patients have been shown to have an increased fracture risk when compared to non-T2D-patients. This research indicates that T2D does not impair the mechanical properties of trabecular bone from the femoral heads of T2D-patients, suggesting that other mechanisms may be responsible for the increased fracture risk seen in T2D-patients.

Introduction. Postvoid residualurine (PVR) can be an unknown chronic disorder, but it can also occur after surgery. A pilot-study initiated in Elective Surgery Center, Silkeborg led to collaboration with a urologist to develop a flowchart regarding treatment of PVR. Depending on the severity, men with significant PVR volumes were either recommend follow up by general practitioner or referred to an urologist for further diagnose and/or treatment. Aim: to determine the prevalence of pre- and postoperative PVR in men >65 years undergoing orthopedic surgeries and associated risk factors. Method. A single-center, prospective cohort study. Male patients were consecutively included during one year from April 2022. Data was extracted from the electronic patient files: age, lower urinary tract symptoms (LUTS), co-morbidity (e.g. diabetes), type of surgery and anesthesia, opioid use, pre- and postoperative PVR. Result. 796 participants; 316 knee-, 276 hip-, 26 shoulder arthroplasties and 178 lower back spinal surgeries. 95% (755) were bladder scanned preoperatively. 12% (89) had PVR 150-300ml, and 3% (23) had PVR >300ml. There was a higher risk of preoperative PVR ≥150ml in patients reporting LUTS, OR 1.97(1.28;3.03), having known neurological disease, OR 3.09(1.41;6.74), and the risk increased with higher age, OR 1.08 per year (1.04;1.12). Diabetes and the type of surgery was not associated with higher risk of PVR. 72% (569) had a postoperative bladder scan. 15% (95%CI: 12-19%) (70) patients without PVR preoperatively had PVR ≥150ml postoperatively. Conclusion. Approximately 15% of the men had PVR ≥150ml preoperatively. Neurological disease was the most severe risk factor and secondary if reporting LUTS. As expected, the risk increased with age. Neither diabetes nor the type of surgery was associated with higher risk. 15% of men without preoperative PVR had PVR after surgery. It is not possible to conclude if it is transient or chronic but further studies are ongoing

Despite the major advances in osteosynthesis after trauma, there remains a small proportion of patients (<10%) who exhibit delayed healing and/or eventual progression to non-union. While known risk factors exist, e.g. advanced age or diabetes, the exact molecular mechanism underlying the impaired healing is largely unknown and identifying which specific patient will develop healing complications is still not possible in clinical practice. The talk will cover our novel multimodal approaches in small animals, which have the potential to precisely capture and understand biological changes during fracture healing on an individual basis. Via combining emerging omics technologies with our recently developed femur defect loading equipment in mice, we provide a platform to precisely link mechanical and molecular analyses during fracture healing

The ability of the body to constantly maintain metabolism homeostasis while fulling the heightened energy and macromolecule demand is crucial to ensure successful tissue healing outcomes. Studies investigating the local metabolic environment during healing are scarce to date. Here, using Type 2 Diabetes (T2D) as a study model, we investigate the impact of metabolism dysregulation on scaffold-guided large-volume bone regeneration. Our study treated wild-type or T2D rats with 5 mm critical-sized femoral defects with 3D-printed polycaprolactone (PCL) scaffolds with 70% porosity. Metabolomics was leveraged for a holistic view of metabolism alteration as healing progress and correlated to regenerated bone tissue volume and quality assessed using micro-computed tomography (µ-CT), histology, and immunohistology. Semi-targeted metabolomics analysis indicated dysregulation in the glycolysis and TCA cycle – the main energy production pathways, in T2D compared to healthy animals. The abundance of metabolites substrates, i.e., amino acids – for protein/ extracellular matrix synthesis was also affected in T2D. Tissue-level metabolites observations aligned with morphological observation with less newly formed bone observed in T2D than wild-type rats. This study enlightens the metabolism landscape during scaffold-guided large-volume bone regeneration in wild-type vs. T2D to further guide the personalization of the scaffold to drive successful regeneration

Bone regeneration is pivotal for the healing of fractures. In case this process is disturbed a non-union can occur. This can be induced by environmental factors such as smoking, overloading etc. Co-morbidities such as diabetes, osteoporosis etc. may be more intrinsic factors besides other disturbances in the process. Those pathways negatively influence the bone regeneration process. Several intrinsic signal transduction pathways (WNT, BMP etc.) can be affected. Furthermore, on the transcriptional level, important mRNA expression can be obstructed by deregulated miRNA levels. For instance, several miRNAs have been shown to be upregulated during osteoporotic fractures. They are detrimental for osteogenesis as they block bone formation and accelerate bone resorption. Modulating those miRNAs may revert the physiological homeostasis. Indeed, physiological fracture healing has a typical miRNA signature. Besides using molecular pathways for possible treatment of non-union fractures, providing osteogenic cells is another solution. In 5 clinical cases with non-union fractures with defects larger than 10 cm, successful administration of a 3D printed PCL-TCP scaffold with autologous bone marrow aspirate concentrate and a modulator of the pathogenetic pathway has been achieved. All patients recovered well and showed a complete union of their fractures within one year after start of the regenerative treatment. Thus, non-union fractures are a diverse entity. Nevertheless, there seem to be common pathogenetic disturbances. Those can be counteracted at several levels from molecular to cell. Compositions of those may be the best option for future therapies. They can also be used in a more personalized fashion in case more specific measurements such as miRNA signature and stem cell activity are applied

Infections in spine surgery are relatively common and devastating complications, a significant burden to the patient and the healthcare system. Usually, the treatment of SSIs consists of aggressive and prolonged antibiotic therapy, multiple debridements, and in chronic cases, hardware removal. Infections are correlated with worse subjective outcomes and even higher mortality. Depending on the type of spine surgery, the infection rate has been reported to be as higher as 20%. Recently silver-coated implants have been introduced in spine surgery to reduce the incidence of post-operative infections and to improve implant survivorship. The aim of the present study is to evaluate complications and outcomes in patients treated with silver-coated implants because of spine infection. All consecutive patients who had spine stabilization with a silver-coated implant from 2018 to 2021 were screened for inclusion in the study. Inclusion criteria were: (1) six months of minimum follow-up; (2) previous surgical site infection; hematogenous spondylodiscitis requiring surgical stabilization. Demographic and surgical information were obtained via chart review, all the device-related complications and the reoperation rate were also reported. A total of 57 patients were included in the present study. The mean age was 63.4 years, and there were 36 (63%) males and 21 (37%) females. Among the included cases, 57% were SSIs, 33% were spondylodiscitis, and 9% were hardware mobilization. Comorbidities such as diabetes mellitus, obesity, smoke, and oncological history were significant risk factors. In addition, the organisms cultured were Staphylococcus species in most of the cases. At six months of follow-up, 40% of patients were considered free from infection, while 20% needed multiple surgeries. The present research showed satisfactory results of silver-coated implants for the treatment of spine infection

Introduction. Diabetes mellitus type 2 (DMT2) patients often develop Achilles tendon (AS) degeneration. The ZDF rat model is often used to study DMT2. Hence, this study investigated whether tenocytes isolated from diabetic and non diabetic ZDF rats respond differentially to normo- (NG) and hyperglycemic (HG) conditions in the presence of tumor necrosis (TNF)α. Method. AS tenocytes isolated from adult diabetic (fa/fa) or lean (fa/+) Zucker Diabetic Fatty (ZDF) rats were treated with 10 ng/mL TNFα either under NG or HG conditions (1 g/L versus 4.5 g/L glucose). Tendons were characterized histopathologically using Movin score. Tenocyte survival, metabolic activity, gene and/or protein expression of the main tendon extracellular matrix (ECM) component collagen type 1, the myofibroblast marker alpha smooth muscle actin (αSMA, Acta2), complement regulatory factors, the antioxidant defense enzyme heme oxygenase-1 (Hmox1), suppressors of cytokine signaling (Socs)1 and Soc3 were analyzed. Result. Tendons of diabetic rats showed significantly higher Movin score values suggesting tendon degeneration. Tenocyte vitality remained high, but metabolic activity was impaired by HG conditions, irrespectively of tenocyte origin. Higher amounts of αSMA were visualized in tendons/cells of diabetic rats or those exposed to TNFα. Collagen type 1 protein and gene expression was suppressed by TNFα (NG), but only in cells of non diabetic animals. The anaphylatoxin receptor C3aR was higher expressed in tenocytes from diabetic animals. CD46 was suppressed by TNFα (NG) in cells of diabetic rats. Hmox1, Socs1 and Socs3 were induced by HG, but only in tenocytes of diabetic rats (4 h). Conclusion. The response of tenocytes to TNFα depends on glucose supply and cell origin suggesting their irreversible impairment in DMT2

We investigated factors associated with postoperative lipiduria and hypoxemia in patients undergoing surgery for orthopedic fractures. We enrolled patients who presented to our emergency department due to traumatic fractures between 2016 and 2017. We collected urine samples within 24 hours after the patients had undergone surgery to determine the presence of lipiduria. Hypoxemia was defined as an SpO2 <95% determined with a pulse oximeter during the hospitalization. Patients’ anthropometric data, medical history, and laboratory test results were collected from the electronic medical record. Logistic regression analyses were used to determine the associations of clinical factors with postoperative lipiduria and hypoxemia with multivariate adjustment. A total of 144 patients were analyzed (mean age 51.3 ± 22.9 years, male 50.7%). Diabetes (odd ratio 3.684, 95% CI 1.256-10.810, p=0.018) and operation time (odd ratio 1.005, 95% CI 1.000-1.009, p=0.029) were independently associated with postoperative lipiduria, while age (odd ratio 1.034, 95% CI 1.003-1.066, p=0.029), body mass index (odd ratio 1.100, 95% CI 1.007-1.203, p=0.035), and operation time (odd ratio 1.005, 95% CI 1.000-1.010, p=0.033) were independently associated with postoperative hypoxemia. We identified several factors independently associated with postoperative lipiduria and hypoxemia in patients with fracture undergoing surgical intervention. Operation time was associated with both postoperative lipiduria and hypoxemia, and we recommend that patients with prolonged operation for fractures should be carefully monitored for clinical signs related to fat embolism syndrome

A Morel-Lavallee lesion (MLL) is a benign cystic lesion that occurs due to injury to the soft-tissue envelope's perforating vascular and lymphatic systems, resulting in a distinctive hemolymphatic fluid accumulation between the tissue layers. The MLL has the potential to make a significant impact on the treatment of orthopaedic injuries. A 79-year-old male patient community ambulatory with assisting aid (cane) known case of Diabetes mellitus, hypertension, bronchial asthma and ischemic heart disease. He was brought to the Emergency, complaining of right hip discomfort and burning sensation for the last 5 days with no history of recent trauma at all. Patient had history of right trochanteric femur fracture 3 years ago, treated with DHS in a privet service. Clinical and Radiological assessment showed that the patient mostly has acute MLL due to lag screw cut out. We offered the patient the surgical intervention, but he refused despite explaining the risks of complications if not treated and preferred to receive the conservative treatment. Compression therapy management explained to him including biker's shorts (instructed to be worn full-time a day) and regular follow up in clinic. Symptom's improvement was reported by the patient in the subsequent visits. In the polytrauma patient, a delayed diagnosis of these lesions is conceivable due to the presence of more visible injuries. It's located over the greater trochanter more commonly, but sometimes in other areas such as the lower lumbar region, the thigh, or the calf. Incorrect or delayed diagnosis and care can have unfavorable outcomes such as infection, pseudocyst development, and cosmetologically deformity. Magnetic resonance imaging (MRI) and ultrasound will aid in MLL diagnosis. However, the effectiveness of MLL therapy remains debatable. We strongly believe that the MLL caused due to tangential shear forces applied to the soft tissue leads to accumulation of the blood and/or lymph between the subcutaneous and overlying fascia and it often misdiagnosed due to other distracting injuries. Nontheless, in our case we reported MLL occur due to internal pressure on the fascia caused by cut out of DHS lag screw

To determine risk factors of infection in total knee arthroplasty. This descriptive study was conducted in the Department of Orthopedics for a duration of three years from January 2016 to January 2019. All patients undergoing primary total knee replacement were included in the study. Exclusion criteria were all patients operated in another hospital and revision total knee replacement. All patients were followed up at 2, 4, 8, 12 and 24 weeks post-operatively. Signs of inflammation and inflammatory markers such as total leukocyte count (TLC), C-reactive protein (CRP) and ESR were measured. Risk factors like age, body mass index (BMI), ASA, co-morbid conditions were also noted. A total of 78 patients underwent primary unilateral Total Knee Replacement (TKR) during the study period. Of these, 30 (34.09%) were male and 48 (61.54%) female patients. Mean age of patients was 68.32 ± 8.54 years. Average BMI 25.89 Kg/m2 .Osteoarthritis was the pre-dominant cause of total knee replacement (94.87%). Among co-morbid factors 33.33% were diabetic, 28.20% having ischemic heart disease and 12.82% with chronic lung disease. Upon anaesthesia fitness pre-operatively, 91.02% patients had an American society of anaesthesiologist score (ASA) between 0–2 while 07 (8.97%) between 3- 5. Average duration of surgery was 85.62± 4.11 minutes. 6.41% cases got infected. In majority of the infected cases (60%), Staphylococcus aureus was the infective organism. Diabetes Mellitus (p=0.01) and Obesity (p=0.02) had a significant relation to post-operative infection. Pre-operative risk evaluation and prevention strategies along with early recognition of infection and control can greatly reduce the risk of joint infection post-TKR which will not only improve the mobility of patient but also its morbidity and mortality as well. Key Words:. C-reactive protein (CRP), Erythrocyte Sedimentation Rate (ESR), Staphylococcus aureus, Total Knee Arthroplasty (TKA)

Introduction. Unplanned reoperations (UROs) following corrective surgery for adult spinal deformity (ASD) present significant challenges for both patients and surgeons. Understanding the specific UROs types is crucial for improving patient outcomes and refining surgical strategies in ASD correction. Method. This retrospective analysis utilized data from the American College of Surgeons National Surgical Quality Improvement Program (ACS NSQIP) database spanning from 2017 to 2021. Patient information was extracted using specific CPT codes related to posterior pedicle fixation. Result. In a cohort of 1088 patients undergoing posterior spinal deformity corrections, we examined various preoperative factors to discern their correlation with reoperation prevalence. Our analysis revealed no statistically significant differences in reoperation prevalence concerning gender (male: 4.0%, p=0.131) or ethnicity (Hispanic: 4.2%, p=0.192). Similarly, no notable associations were identified for diabetes mellitus, smoking status, dyspnea, history of severe COPD, hypertension, ASA classification, or functional health status before surgery, with reoperation prevalences ranging from 3.2% to 8.8% and p-values spanning from 0.146 to 0.744. Overall, the reoperation prevalence within the entire cohort stood at 5.2% (55 cases). In terms of the types of reoperations investigated, spinal-related procedures emerged as the most prevalent, accounting for 43.7% (24 cases), followed closely by wound site revisions at 23.6% (13 cases). Additionally, gastrointestinal-related procedures and various other miscellaneous interventions, such as uroscopy, demonstrated reoperation prevalences of 7.2% (4 cases) and 25.5% (14 cases), respectively. Conclusion. our findings highlight the diverse spectrum of reoperation procedures encountered following posterior spinal deformity corrections, with wound site revisions and spinal-related interventions being the most prevalent categories. These results emphasize the complexity of managing UROs in spinal surgery and the need for tailored approaches and infection/incision protocols to address the specific challenges associated with each type of reoperation