No changes in bone mineral density following total knee arthroplasty using an all-polyethylene tibial component.

PURPOSE: Polyethylene particles produced from metal-backed tibial (MBT) implants are understood to contribute to bone loss and component loosening. This, along with advanced surgical techniques, improved materials and increasing costs, has renewed interest in all-polyethylene tibias (APTs). We investigated peri-APT bone mineral density (BMD) in patients, expecting to find no differences between two post-operative values. METHODS: Patients over 65 years, with BMI ≤ 37.5 kg/m2 and no previous joint replacements were recruited to have computer-navigated total knee arthroplasty using an APT. The study cohort (n = 27) had mean age of 71.9 (SD 4.35) and BMI of 31.2 (SD 3.8). The BMD examinations were performed 6 weeks and 18 months post-operatively. Six regions of interest (ROI) were identified on anterior/posterior and lateral dual-energy X-ray absorptiometry scans. For each ROI, BMD relative differences (RDs) were determined between limbs and RDs at the two time points were compared. RESULTS: No differences were found between the RDs for any ROI. No revisions or complications were reported. At 18 months post-operatively, 79.2% of the cohort were very satisfied or satisfied with the outcome of their surgery and Oxford Knee Scores improved significantly compared to pre-operatively (p < 0.001). Mean knee range of motion was 102° (SD 10.7°), and mean leg alignment was 2.0° valgus (1-6°valgus). CONCLUSION: Results from BMD analysis suggest that implants were well fixated without compromising function. We believe that using APTs with computer navigation is a viable cheaper option to MBTs for patients who are less active, have lower BMI and good bone quality.

Plasma IGFBP-2 levels reveal heterogeneity in hepatic fat content in adults with excess visceral adiposity.

Lay summary: Obesity is frequently accompanied by a fatty liver. However, some individuals with high abdominal fat levels nevertheless have low levels of liver fat. Reasons for such discordant phenotypes are unclear. In this paper, we report that among asymptomatic individuals with high levels of visceral fat, low concentrations of IGFBP-2 in the circulation were associated with significantly higher hepatic fat content compared to those with high IGFBP-2 levels. We conclude that quantification of plasma IGFBP-2 concentrations may be useful to identify the early risk for liver fat accumulation in apparently healthy individuals without cardiovascular symptoms. Aim/hypothesis: Although excess visceral adiposity (VAT) is generally associated with increased liver fat (LF), recent evidence has revealed heterogeneity in LF content among adults with visceral obesity, potentially contributing to specific differences in cardiometabolic outcomes. Reasons for such discordant VAT-LF phenotypes are largely unknown. The present study aimed at assessing whether circulating levels of insulin growth-factor binding protein-2 (IGFBP-2) could be a useful biomarker in the identification of heterogenous and discordant VAT-LF phenotypes. Methods: A sample of 308 middle-aged Caucasian apparently healthy men and women without cardiovascular symptoms were studied for the present cross-sectional analyses. Fasting plasma glucose and lipid levels were assessed and an oral glucose tolerance test was performed. Hepatic fat fraction (HFF) was measured using magnetic resonance spectroscopy whereas VAT was assessed by magnetic resonance imaging. Plasma IGFBP-2 levels were quantified by ELISA. Participants were then classified on the basis of median VAT (81 mL) and IGFBP-2 levels (233 ng/mL). Results: Individuals with high levels of VAT were characterized by higher waist circumference, lower insulin sensitivity, as well as by higher plasma triglyceride and lower HDL-cholesterol levels. Plasma IGFBP-2 levels were inversely correlated with HFF (r = -0.39, p < 0.0001). Among men and women with high levels of VAT, those with low levels of IGFBP-2 had significantly higher HFF (7.5 ± 0.7%), compared to participants with high IGFBP-2 concentrations (3.2 ± 0.5%, p < 0.0001). Conclusion: In the presence of excess VAT, high IGFBP-2 concentrations are associated with low levels of LF. Although additional studies will be necessary to establish causality and further clarify the clinical implications of these observations, these findings are concordant with a novel function of IGFBP-2 in modulating susceptibility to non-alcoholic fatty liver disease (NAFLD) in the presence of visceral obesity.

Associations of insulin-like growth factor binding protein-2 with metabolic profile and hepatic fat deposition in asymptomatic men and women.

Low circulating levels of insulin-like growth-factor binding protein-2 (IGFBP-2) have been associated with increased adiposity and metabolic alterations such as insulin resistance, dyslipidemia, and nonalcoholic fatty liver disease in individuals with obesity. However, whether IGFBP-2 affects energy metabolism in the early stages of these disorders remains unclear. Herein, we hypothesized that plasma IGFBP-2 concentrations are inversely associated with early liver fat accumulation and alterations in lipid and glucose homeostasis in apparently healthy and asymptomatic men and women. Three hundred thirty-three middle-aged Caucasian men and women apparently healthy and without cardiovascular symptoms were enrolled for a cross-sectional cardiometabolic imaging study. Individuals with BMI ≥ 40 kg/m2, cardiovascular disease, dyslipidemia, hypertension, and diabetes were excluded. Fasting glucose and lipid profiles were measured and an oral glucose tolerance test was performed. Liver fat content was assessed by magnetic resonance spectroscopy. Volume of visceral adipose tissue (VAT) was evaluated by magnetic resonance imaging. Plasma IGFBP-2 levels were quantified by ELISA. Participants with low IGFBP-2 levels were characterized by a higher body fat mass (P < 0.0001), insulin resistance (P < 0.0001), higher plasma triglyceride (TG) (P < 0.0001), and lower HDL-cholesterol levels (P < 0.0001) in a sex-independent manner. IGFBP-2 levels were inversely correlated with hepatic fat fraction in both men (r = -0.36, P < 0.0001) and women (r = -0.40, P < 0.0001). IGFBP-2 concentrations were negatively associated with hepatic fat fraction independently of age and VAT in both men (R2 = 0.23, P = 0.012) and women (R2 = 0.27, P = 0.028). In conclusion, our findings show that even in asymptomatic, apparently healthy individuals, low IGFBP-2 levels are associated with a more deteriorated cardiometabolic risk profile and with a high hepatic fat content in a VAT-independent manner. However, IGFBP-2 does not appear to influence the established sexual dimorphism observed for metabolic variables and hepatic fat fraction. Additional studies are required to better understand the relationships between IGFBP-2 and liver fat content.NEW & NOTEWORTHY Faced with a paucity of reliable clinical etiologic markers for fatty liver, this research article demonstrates, for the first time, that low blood levels of the protein IGFBP-2 are associated with a more deteriorated cardiometabolic risk profile and with a high hepatic fat content independently of visceral fat volume and sex, even in asymptomatic, apparently healthy individuals.

Are all parental experiences equal?: Cluster analysis of salivary cortisol and perception of parental stress in mothers of children with autism spectrum disorder.

Many parents of children with autism spectrum disorder (ASD) report high stress levels related to their parenting role. The experience of stress is reflected in physical symptoms and well-being, as observed by abnormal patterns of cortisol regulation. However, it may be a mistake to conceive parenthood as unilaterally stressful as diverse experiences are possible. Mothers of children with ASD provided salivary cortisol samples and self-rated parental stress. The area under the curve with respect to ground was calculated in regard to three daily collection time points. As a group, mothers reported average levels of parenting stress and flat daily cortisol output. The current age of the child and age at the time of diagnosis moderately predicted overall daily cortisol. Hierarchical clusters analysis identified four distinct profiles of stress regulation based on daily cortisol regulation and perception of parental stress. Groups did not differ based on the severity of symptoms related to autism or demographic information. We suggest that other variables, such as stress mediators and secondary stressors, may explain variability in stress regulation. Future research and intervention should perceive the parental experience as heterogeneous and focus on individualizing the support offered in light of diverse experiences.

Methods to extract and study the biological effects of murine gut microbiota using Caenorhabditis elegans as a screening host.

Gut microbiota has been established as a main regulator of health. However, how changes in gut microbiota are directly associated with physiological and cellular alterations has been difficult to tackle on a large-scale basis, notably because of the cost and labor-extensive resources required for rigorous experiments in mammals. In the present study, we used the nematode Caenorhabditis elegans as a model organism to elucidate microbiota-host interactions. We developed a method to extract gut microbiota (MCB) from murine feces, and tested its potential as food source for and its impact on C. elegans biology compared to the standard bacterial diet Escherichia coli OP50. Although less preferred than OP50, MCB was not avoided but had a lower energy density (triglycerides and glucose). Consistently, MCB-fed worms exhibited smaller body length and size, lower fertility, and lower fat content than OP50-fed worms, but had a longer mean lifespan, which resembles the effects of calorie restriction in mammals. However, these outcomes were altered when bacteria were inactivated, suggesting an important role of symbiosis of MCB beyond nutrient source. Taken together, our findings support the effectiveness of gut MCB processing to test its effects in C. elegans. More work comparing MCB of differently treated mice or humans is required to further validate relevance to mammals before large-scale screening assays.

Perioperative air travel increases the risk of venous thromboembolism following lower limb arthroplasty.

PURPOSE: Venous thromboembolism (VTE) is a significant complication following lower limb arthroplasty (LLA). There is a paucity of evidence with regard to air travel following LLA. Orthopaedic surgeons are often asked by patients regarding air travel following LLA, and there is a need for evidence to guide these patients. METHODS: This was a retrospective cohort study. We identified two cohorts, one travelling to and from the hospital by air and another, by land. All patients received routine preoperative and post-operative care, and thromboprophylaxis, as per our hospital guidelines. We collected baseline demographics, ASA score and incidence of VTE at 90 days using local patient records and a national joint registry. We also recorded data on flight time and overland distance of travel. RESULTS: Two hundred and forty-three patients travelled by air; mean flight time was 74 min. In total, 5498 patients travelled a mean 25.3 miles over land to the hospital. No differences in baseline demographics or ASA score were observed. Four patients developed a VTE in the flight group, with 32 patients suffering a VTE in the control group. There was a significant difference in the VTE rate between the flight and control groups (p < 0.05); the relative risk of developing a VTE in the flight group was 2.85. CONCLUSIONS: In our cohort, perioperative short haul air travel is associated with an increased risk of VTE at 90 days following LLA. Orthopaedic surgeons must ensure that their patients are cognizant of the risks associated with perioperative air travel and take measures to minimise these risks.

Malat1 deficiency prevents hypoxia-induced lung dysfunction by protecting the access to alveoli.

Hypoxia is common in lung diseases and a potent stimulator of the long non-coding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1). Herein, we investigated the impact of Malat1 on hypoxia-induced lung dysfunction in mice. Malat1-deficient mice and their wild-type littermates were tested after 8 days of normoxia or hypoxia (10% oxygen). Hypoxia decreased elastance of the lung by increasing lung volume and caused in vivo hyperresponsiveness to methacholine without altering the contraction of airway smooth muscle. Malat1 deficiency also modestly decreased lung elastance but only when tested at low lung volumes and without altering lung volume and airway smooth muscle contraction. The in vivo responsiveness to methacholine was also attenuated by Malat1 deficiency, at least when elastance, a readout sensitive to small airway closure, was used to assess the response. More impressively, in vivo hyperresponsiveness to methacholine caused by hypoxia was virtually absent in Malat1-deficient mice, especially when hysteresivity, a readout sensitive to small airway narrowing heterogeneity, was used to assess the response. Malat1 deficiency also increased the coefficient of oxygen extraction and decreased ventilation in conscious mice, suggesting improvements in gas exchange and in clinical signs of respiratory distress during natural breathing. Combined with a lower elastance at low lung volumes at baseline, as well as a decreased propensity for small airway closure and narrowing heterogeneity during a methacholine challenge, these findings represent compelling evidence suggesting that the lack of Malat1 protects the access to alveoli for air entering the lung.

Associations between insulin-like growth factor binding protein-2 and lipoprotein kinetics in men.

Low circulating concentrations of insulin-like growth factor binding protein-2 (IGFBP-2) have been associated with dyslipidemia, notably with high triglyceride (TG) levels. However, the determinants by which IGFBP-2 influences lipoprotein metabolism, especially that of TG-rich lipoproteins (TRLs), are poorly understood. Here, we aimed to assess the relationships between IGFBP-2 levels and lipoprotein production and catabolism in human subjects. Fasting IGFBP-2 concentrations were measured in the plasma of 219 men pooled from previous lipoprotein kinetics studies. We analyzed production rate and fractional catabolic rates of TRLapoB-48, and LDL-, IDL-, and VLDLapoB-100 by multicompartmental modeling of l-[5,5,5-D3] leucine enrichment data after a 12 h primed constant infusion in individuals kept in a constant nutritional steady state. Subjects had an average BMI of 30 kg/m2, plasma IGFBP-2 levels of 157 ng/ml, and TG of 2.2 mmol/l. After adjustments for age and BMI, IGFBP-2 levels were negatively associated with plasma TG (r = -0.29; P < 0.0001) and positively associated with HDL-cholesterol (r = 0.26; P < 0.0001). In addition, IGFBP-2 levels were positively associated with the fractional catabolic rate of VLDLapoB-100 (r = 0.20; P < 0.01) and IDLapoB-100 (r = 0.19; P < 0.05) and inversely with the production rate of TRLapoB-48 (r = -0.28; P < 0.001). These correlations remained statistically significant after adjustments for age, BMI, and the amount of fat given during the tracer infusion. These findings show that the association between low plasma IGFBP-2 and high TG concentrations could be due to both an impaired clearance of apoB-100-containing VLDL and IDL particles and an increased production of apoB-48-containing chylomicrons. Additional studies are necessary to investigate whether and how IGFBP-2 directly impacts the kinetics of TRL.

IGFBP-2 partly mediates the early metabolic improvements caused by bariatric surgery.

Insulin-like growth factor-binding protein (IGFBP)-2 is a circulating biomarker of cardiometabolic health. Here, we report that circulating IGFBP-2 concentrations robustly increase after different bariatric procedures in humans, reaching higher levels after biliopancreatic diversion with duodenal switch (BPD-DS) than after Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG). This increase is closely associated with insulin sensitization. In mice and rats, BPD-DS and RYGB operations also increase circulating IGFBP-2 levels, which are not affected by SG or caloric restriction. In mice, Igfbp2 deficiency significantly impairs surgery-induced loss in adiposity and early improvement in insulin sensitivity but does not affect long-term enhancement in glucose homeostasis. This study demonstrates that the modulation of circulating IGFBP-2 may play a role in the early improvement of insulin sensitivity and loss of adiposity brought about by bariatric surgery.

T cells accumulate in non-diabetic islets during ageing.

BACKGROUND: The resident immune population of pancreatic islets has roles in islet development, beta cell physiology, and the pathology of diabetes. These roles have largely been attributed to islet macrophages, comprising 90% of islet immune cells (in the absence of islet autoimmunity), and, in the case of type 1 diabetes, to infiltrating autoreactive T cells. In adipose, tissue-resident and recruited T and B cells have been implicated in the development of insulin resistance during diet-induced obesity and ageing, but whether this is paralleled in the pancreatic islets is not known. Here, we investigated the non-macrophage component of resident islet immune cells in islets isolated from C57BL/6 J male mice during ageing (3 to 24 months of age) and following similar weight gain achieved by 12 weeks of 60% high fat diet. Immune cells were also examined by flow cytometry in cadaveric non-diabetic human islets. RESULTS: Immune cells comprised 2.7 ± 1.3% of total islet cells in non-diabetic mouse islets, and 2.3 ± 1.7% of total islet cells in non-diabetic human islets. In 3-month old mice on standard diet, B and T cells each comprised approximately 2-4% of the total islet immune cell compartment, and approximately 0.1% of total islet cells. A similar amount of T cells were present in non-diabetic human islets. The majority of islet T cells expressed the αß T cell receptor, and were comprised of CD8-positive, CD4-positive, and regulatory T cells, with a minor population of γδ T cells. Interestingly, the number of islet T cells increased linearly (R2 = 0.9902) with age from 0.10 ± 0.05% (3 months) to 0.38 ± 0.11% (24 months) of islet cells. This increase was uncoupled from body weight, and was not phenocopied by a degree similar weight gain induced by high fat diet in mice. CONCLUSIONS: This study reveals that T cells are a part of the normal islet immune population in mouse and human islets, and accumulate in islets during ageing in a body weight-independent manner. Though comprising only a small subset of the immune cells within islets, islet T cells may play a role in the physiology of islet ageing.

Circulating IGFBP-2 levels reveal atherogenic metabolic risk in schizophrenic patients using atypical antipsychotics.

OBJECTIVES: Second generation antipsychotics (SGAs) induce weight gain and dyslipidemia, albeit with important intervariability. Insulin-like growth factor binding protein (IGFBP)-2 is proposed as a circulating biomarker negatively associated with waist circumference and hypertriglyceridemia. Thus, we tested whether metabolic alterations developed upon the use of SGAs are associated with plasma IGFBP-2 levels. METHODS: A cross-sectional study was performed in 87 men newly diagnosed with schizophrenia and administered for approximately 20 months with olanzapine or risperidone as their first antipsychotic treatment. Plasma IGFBP-2 concentration, anthropometric data, as well as glucose and lipid profiles were determined at the end of the treatments. RESULTS: IGFBP-2 levels were similar between patients using olanzapine or risperidone and were negatively correlated with waist circumference, insulin sensitivity, and plasma triglycerides (TG). A higher proportion of men with a hypertriglyceridemic (hyperTG) waist phenotype was found in patients with IGFBP-2 levels lower than 220 ng/mL (43% for olanzapine and 13% for risperidone) compared to those with IGFBP-2 above this threshold (10% and 0%, respectively). CONCLUSIONS: IGFBP-2 may have a role in altering metabolic risk in schizophrenic patients using SGAs. Longitudinal studies are required to evaluate whether IGFBP-2 can predict the development of a hyperTG waist phenotype in this population.

Human Brown Adipocyte Thermogenesis Is Driven by ß2-AR Stimulation.

Stimulation of brown adipose tissue (BAT) thermogenesis in humans has emerged as an attractive target to improve metabolic health. Pharmacological stimulations targeting the ß3-adrenergic receptor (ß3-AR), the adrenergic receptor believed to mediate BAT thermogenesis, have historically performed poorly in human clinical trials. Here we report that, in contrast to rodents, human BAT thermogenesis is not mediated by the stimulation of ß3-AR. Oral administration of the ß3-AR agonist mirabegron only elicited increases in BAT thermogenesis when ingested at the maximal allowable dose. This led to off-target binding to ß1-AR and ß2-AR, thereby increasing cardiovascular responses and white adipose tissue lipolysis, respectively. ADRB2 was co-expressed with UCP1 in human brown adipocytes. Pharmacological stimulation and inhibition of the ß2-AR as well as knockdown of ADRB1, ADRB2, or ADRB3 in human brown adipocytes all confirmed that BAT lipolysis and thermogenesis occur through ß2-AR signaling in humans (ClinicalTrials.govNCT02811289).

3D biofabrication for soft tissue and cartilage engineering.

Soft tissue injuries (STIs) affect patients of all age groups and represent a common worldwide clinical problem, resulting from conditions including trauma, infection, cancer and burns. Within the spectrum of STIs a mixture of tissues can be injured, ranging from skin to underlying nerves, blood vessels, tendons and cartilaginous tissues. However, significant limitations affect current treatment options and clinical demand for soft tissue and cartilage regenerative therapies continues to rise. Improving the regeneration of soft tissues has therefore become a key area of focus within tissue engineering. As an emerging technology, 3D bioprinting can be used to build complex soft tissue constructs "from the bottom up," by depositing cells, growth factors, extracellular matrices and other biomaterials in a layer-by-layer fashion. In this way, regeneration of cartilage, skin, vasculature, nerves, tendons and other bodily tissues can be performed in a patient specific manner. This review will focus on recent use of 3D bioprinting and other biofabrication strategies in soft tissue repair and regeneration. Biofabrication of a variety of soft tissue types will be reviewed following an overview of available cell sources, bioinks and bioprinting techniques.

Metabolic adaptations after bariatric surgery: adipokines, myokines and hepatokines.

This review addresses the impact of bariatric surgery on the endocrine aspects of white adipose tissue, muscle and the liver. We describe literature supporting the notion that adipokines, myokines and hepatokines likely act in concert and drive many of the long-term metabolic improvements following surgery. Circulating adiponectin is increased while secretion of pro-inflammatory interleukins (1, 6 and 8) decreases, alongside leptin secretion. The metabolic improvements observed in the muscle might relate to reduction of myokines contributing to insulin resistance (including myostatin, brain-derived neurotrophic factor and fibroblast growth factor-21). Subject to exception, hepatokine secretion is generally increased (such as insulin-like growth factor-binding protein 2, adropin and sex hormone-binding globulin). In conclusion, bariatric surgery restores metabolic functions by enhancing the time-dependent secretion of anti-inflammatory, insulin-sensitizing and antilipemic factors. Further research is needed to understand the molecular mechanisms by which these factors may trigger the remission of obesity-related comorbidities following bariatric surgery.

Differential Effects of Long-Term Caloric Restriction and Dietary Protein Source on Bone and Marrow Fat of the Aging Rat.

Long-term caloric restriction (CR) has been shown to be beneficial to various tissues and organs. In contrast, CR exerts differential effects on bone, which could be due in part to the nature of the protein regime utilized. Male Sprague Dawley rats (8-month-old) were subjected for 12 months to 40% CR in macronutrients and compared with rats fed ad libitum for the same period. Casein- and soy-fed groups were compared. There was a significant decrease in bone quality in both CR groups, which was independent of the source of protein in the diet. In contrast, the group fed soy protein ad libitum showed better bone quality and higher levels of bone formation compared with casein-fed animals. Notably, bone marrow adipocytes were not mobilized upon CR as demonstrated by an absence of change in adipocyte number and tissue expression of leptin. This study demonstrates that the negative effect of CR on bone quality could not be prevented by the most common protein regimes.

Technical and surgical causes of outliers after computer navigated total knee arthroplasty.

BACKGROUND: Navigated total knee arthroplasty (TKA) improves implant and limb alignment but outliers continue to exist. This study aimed to determine the technical and surgical causes of outliers. METHODS: This retrospective cohort study included 208 patients who had undergone navigated TKA. Limb and implant alignment indices were measured on post-operative CT scans: mechanical femoro-tibial angle (MFTA); coronal femoral angle (CFA); coronal tibial angle (CTA); sagittal femoral angle (SFA); and sagittal tibial angle (STA). Values outside 0°±3° for MFTA and SFA, 90°±3° for CFA, CTA and STA were considered outliers. Intra-operative navigation data and CT scans were evaluated to categorize the causes of sagittal and coronal plane outliers into hip centre error; ankle centre error; heterogeneous tibial cement mantle; malalignment accepted by surgeon; suboptimal knee balance; and no obvious explanation. RESULTS: Of the 1040 measurements (five per TKA), the overall incidence of outliers was 10.4% (n = 108). Femoral component outliers (CFA + SFA, n = 51) were all attributable to hip centre error. Tibial component outliers (CTA + STA, n = 43) were attributable to ankle centre error (n = 6), heterogeneous cement mantle (n = 20), malalignment accepted by the surgeon (n = 6) and no obvious cause (n = 11). MFTA outliers were attributable to hip centre error (n = 4) or suboptimal knee balance (n = 10). CONCLUSIONS: Surgeon related errors can be minimized by a meticulous operative technique. These results indicate scope for additional technical improvement, especially in hip centre acquisition, which may further reduce the incidence of outliers.

Computer assisted orthopaedic surgery: Past, present and future.

Computer technology is ubiquitous and relied upon in virtually all professional activities including neurosurgery, which is why it is surprising that it is not the case for orthopaedic surgery with fewer than 5% of surgeons using available computer technology in their procedures. In this review, we explore the evolution and background of Computer Assisted Orthopaedic Surgery (CAOS), delving into the basic principles behind the technology and the changes in the discussion on the subject throughout the years and the impact these discussions had on the field. We found evidence that industry had an important role in driving the discussion at least in knee arthroplasty-a leading field of CAOS-with the ratio between patents and publications increased from approximately 1:10 in 2004 to almost 1:3 in 2014. The adoption of CAOS is largely restrained by economics and ergonomics with sceptics challenging the accuracy and precision of navigation during the early years of CAOS moving to patient functional improvements and long term survivorship. Nevertheless, the future of CAOS remains positive with the prospect of new technologies such as improvements in image-guided surgery, enhanced navigation systems, robotics and artificial intelligence.

The assessment of instability in the osteoarthritic knee.

Patient-reported instability is a common complaint amongst those with knee arthritis.Much research has examined the assessment of self-reported instability in the knee; however, no definitive quantitative measure of instability has been developed.This review focuses on the current literature investigating the nature of self-reported instability in the arthritic knee and discusses the possibilities of further investigation. Cite this article: EFORT Open Rev 2019;4:70-76. DOI: 10.1302/2058-5241.4.170079.

A new landmark for measuring tibial component rotation after total knee arthroplasty.

BACKGROUND: Existing methods for assessment of total knee arthroplasty (TKA) component rotation on computed tomography (CT) scans are complex, especially in relation to the tibial component. Anecdotal evidence from our practice pointed towards a potential new landmark. The study aims were to check the prevalence of this landmark, define tibial component rotation in relation to it and demonstrate its reliability. METHODS: Two hundred and eleven CTs undertaken following TKA were reviewed for presence of the landmark. A protocol to measure tibial component rotation in relation to this landmark was developed and the rotation measured using this method and Berger's protocol. Thirty one of the 211 CT scans were measured twice by two observers. Reliability was calculated using the Intraclass Correlation Coefficient (ICC). RESULTS: The new landmark of a flat area on the lateral cortex of the tibia inferior to the tibial component was identified on all scans. Median tibial component rotation measured using our protocol was 0.0°â€¯±â€¯5.4° and -9.2°â€¯±â€¯5.5° using Berger's protocol. Intra-observer reliability with the new method was excellent (ICCs of 0.899 and 0.871) and inter-observer reliability was good (ICCs of 0.734 and 0.836). CONCLUSIONS: The new landmark had a very high prevalence and could be used to define tibial component rotation. This measurement of tibial component rotation had acceptable reliability. This landmark has potential for use in the radiological assessment of tibial component rotation following TKA. Further work is required to determine its relationship to anatomical structures and symptoms of tibial component mal-rotation.

Cerebral tissue pO2 response to stimulation is preserved with age in awake mice.

Compromised oxygen supply to cerebral tissue could be an important mechanism contributing to age-related cognition decline. We recently showed in awake mice that resting cerebral tissue pO2 decreases with age, a phenomenon that manifests mainly after middle-age. To extend these findings, here we aimed to study how tissue pO2 response to neuronal stimulation is affected by aging. We used two-photon phosphorescence lifetime microscopy to directly measure the brain tissue pO2 response to whisker stimulation in healthy awake young, middle-aged and old mice. We show that despite a decrease in baseline tissue pO2, the amplitude of the tissue pO2 response to stimulation is well preserved with age. However, the response dynamics are altered towards a slower response with reduced post-stimulus undershoot in older ages, possibly due to stiffer vessel wall among other factors. An estimation of the net oxygen consumption rate using a modified Krogh model suggests that the O2 overshoot during stimulation may be necessary to secure a higher capillary O2 delivery to the tissue proportional to increased CMRO2 to maintain the capillary tissue pO2. It was observed that the coupling between the CMRO2 and capillary O2 delivery is preserved with age.