BACKGROUND AND PURPOSE:A clinical problem in total hip arthroplasty (THA) is periprosthetic osteolysis/aseptic loosening. There is a possible association between periprosthetic osteolysis and higher risk of cardiovascular disease (CVD). The aim of this study was to investigate whether THA patients with asymptomatic periacetabular osteolysis, have an increased long-term risk of CVD compared to THA patients without osteolysis, assess time to the event, and compare possible cardiovascular risk markers between the two groups. PATIENTS AND METHODS:We conducted a retrospective cohort study of 139 patients treated with uncemented THA between 1992 and 2007. All patients were assessed by computed tomography of the affected hip to sort patients in one group with osteolysis and one without. The statistical analysis was based on descriptive statistics. The Kaplan-Meier method was used to estimate time to event and Cox regression models were fitted to calculate crude and adjusted hazard ratios (HR) with 95% confidence intervals (95% CI). RESULTS:There were 33 patients with periacetabular osteolysis and 106 patients without. Mean follow-up time was 16.6 years (range, 12-30). 16 patients (11%) were diagnosed with CVD after a mean (SD) of 14 (6) years, with a higher relative incidence 8/33 (24%) vs 8/106 (8%) of CVD among patients with periacetabular osteolysis. The hazard ratio was 1.6, 95% confidence interval (0.4-5.8). There were no differences in presence of cardiovascular risk markers or ECG abnormalities. INTERPRETATION:We found no association between periacetabular osteolysis and possible risk markers for CVD. There was a trend towards higher incidence of CVD among patients with periacetabular osteolysis. Based on the results from our relatively small cohort it cannot be excluded that low-grade peri-implant inflammation may increase long term risk of CVD following THA.

BACKGROUND:Surgical site infection (SSI) following orthopedic surgery impacts patient outcomes. Airborne transmission is one potential route of infection. Despite their high cost and resource demands, modern ventilation systems have shown limited efficacy in reducing SSI rates. This trial investigated the effectiveness of a low-cost air purifier in reducing SSI rates after orthopedic surgery. METHODS:In a nationwide, multicenter, double-blind, cluster-randomized crossover, placebo-controlled superiority trial, we included all patients undergoing orthopedic surgery during the trial period. The intervention group underwent surgery in operating rooms with active Novaerus NV800 air purifiers, while the control group underwent surgery in operating rooms with the same air purifiers that were inactive. The primary end point was SSI within 12 weeks post surgery, defined as a postsurgery infection marker (PSIM), a custom composite outcome based on registry codes for prescribed antibiotics, diagnoses, and surgical procedures. Logistic regression was performed to evaluate the primary outcome. RESULTS:Of the 40,547 patients analyzed, 19,869 were in the intervention group and 20,678 in the control group. The PSIM rate was 9.2% in the invention group, and 9.4% in the control group, with an odds ratio of 0.98 (95% confidence interval, 0.91 to 1.05) for the intervention group. This finding remained consistent across various subgroups based on diagnoses, hospital levels, and ventilation types. CONCLUSIONS:In modern operating rooms equipped with standard, midrange airflow ventilation systems, the addition of wall-mounted plasma air purifiers did not reduce the PSIM rate after orthopedic surgery. (Funded by the Swedish Research Council; grant number, 2017-00198; ClinicalTrials.gov number, NCT02695368.).

Lubricin/proteoglycan-4 (PRG-4) is a mucinous glycoprotein that lubricates cartilage and maintains normal tissue function and cell homeostasis. Altered O-glycoproteforms of lubricin have been found in osteoarthritis (OA) synovial fluid (SF), which could ostensibly be used to diagnose early onset OA. However, SF is invasive to obtain and generally would not be surveyed from otherwise healthy individuals. Thus, a plasma-based OA screening tool focused on lubricin glycosylation could be a less invasive method to aid in early-stage OA diagnosis. In this report, we used glycomics and glycoproteomics to characterize glycoproteoforms of OA lubricin in SF and plasma. We obtained near-complete sequence coverage of lubricin’s mucin domain and its glycosylation using matched SF and plasma from OA patients (N=5). From SF lubricin we observed a spectrum of O-glycans ranging from a single GalNAcα1-Ser/Thr monosaccharide up to branched pentasaccharides. In contrast, plasma based lubricin was predominantly decorated with sialylated Galβ1-3GalNAcα1-Ser/Thr (Sialyl T). To explain the glycosylation differences observed between SF and plasma lubricin, we present splice variant-specific peptides found within the non-glycosylated region, revealing that that the longest spliceoform of lubricin was present exclusively in SF, while additional shorter splice variants could only be detected in plasma.Based on our glycoproteomic data, we developed and validated a lectin assay for lubricin, and applied this on a larger cohort of matched SF/plasma (N=19) to confirm the glycosylation differences between SF and plasma proteoforms. Next, we leveraged our assay to screen over 100 OA patient samples (OA patients N=108/controls N=38) to probe plasma lubricin as an OA biomarker. Here, we detected a decrease in α2,6 linked sialic acid in OA patients and further show that the extent of α2,6 and α2,3 sialylation on plasma-associated lubricin correlated with patient characteristics, especially Body Mass Index (BMI).

Lubricin or proteoglycan-4 (PRG-4) is a mucinous glycoprotein lubricating the cartilage and maintaining normal tissue function and cell-homeostasis. Altered O -glycoforms of lubricin has been found in osteoarthritis (OA) synovial fluid (SF). Here, we utilized a Fluorescent Immuno-Lectin Assay (FILA) to measure the levels of lubricin glycoforms in plasma/SF and their potential as biomarkers for disease. Five different lectins were used in the assay: Macrophage Galactose-type lectin (MGL), Sambucus Nigra Agglutinin (SNA), Maackia Amurensis Agglutinin (MAA), Peanut Agglutinin (PNA), and Galectin-3 (Gal-3). Our results showed that the levels of lubricin glycoforms in late-stage knee OA plasma (typically <10 μg/ml) are 1-3 order of magnitude lower than in OA SF (typically> 100 μg/ml). Furthermore, plasma lubricin glycans displayed higher level of sialylation, while SF derived lubricin displayed higher level of Tn-antigens. In OA patients we found decreased level in plasma of SNA binding lubricin (p=0.0023) compared to controls. This lectin binds 6 linked sialic acid. In addition, we found that lubricin glycoforms correlated both with Body Mass Index (BMI) and age, especially in regards of sialylation as measured by both MAA and SNA. Our data suggest that glycosylation of lubricin is different comparing SF with plasma. Moreover, the glycosylation of plasma lubricin is altered in OA patients compared controls. ### Competing Interest Statement NGK authored a patent involving the use of lubricin for diagnostics assigned to the company Lynxon AB, and NGK holds equity in Lynxon AB. GJ and TS authored patents related to rhPRG4. GJ and TS hold equity in Lubris BioPharma LLC. TS was also paid consultancy fees by Lubris BioPharma. The remaining authors declare no competing interests. The other authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. ### Funding Statement Financial contribution to NGK from the Swedish state under the agreement between the Swedish government and the county council, the ALF-agreement (ALFGBG-722391), the Swedish Research Council (621-2013-5895), Petrus and Augusta Hedlunds foundation (M-2016-0353), and AA insurance research fund (dnr 150150). GJ was funded from the National Institute of Health R01AR067748. A stipend for ARA was provided from OsloMet. ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: Plasma samples and their controls were from a biobank maintained by Sahlgrenska University hospital (Gothenburg, Sweden). All patients and participants had given informed consent. Ethical permission for patient screening was obtained from the ethical board in Gothenburg, Sweden (ethical application 172-15). Analysis of OA biobank samples in Norway has been ethically approved by the Sor-ost regional ethics commitee (470919) and handling of personal data approved by Norwegian Agency for Shared Services in Education and Research (431575). I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes Analytical data about individual patient FILA results are included in the Supplementary Material. Inquiries about additional patient meta data can be directed to the corresponding author.

Background and purpose: Periprosthetic joint infection (PJI) is a feared complication of arthroplasty surgery. There is controversy as to whether PJI also correlates with increased mortality. Our aim was to investigate in a nationwide cohort if PJI is an independent risk factor for dying. Patients and methods: We performed a retrospective cohort study based on data from the Swedish Hip Arthroplasty Register (SHAR). All patients with a revision THA performed between 1998 and 2017 were included. The outcome is mortality; exposure is PJI according to SHAR. The control group was study participants who underwent aseptic revision. Confounders were age, sex, diagnosis, and comorbidity according to the Elixhauser index. The outcome was analyzed with a Cox proportional hazards model. Results: 4,943 PJI revisions and 12,529 non-infected revisions were included in the analysis. The median follow-up time was 4.1 years. In the PJI group, 1,972 patients died and in the control group, 4,512. The incidence rate ratio was 1.19 (95% confidence interval [CI] 1.13–1.25), the crude hazard ratio (HR) 1.19 (CI 1.13–1.25), and the adjusted HR 1.05 (CI 0.99–1.12) for the exposed versus the unexposed group. The strongest confounder was comorbidity. Conclusion: The increased mortality risk after revision due to PJI is mainly caused by the comorbidity of the patient, rather than by the infection itself.

Introduction There is controversy regarding the importance of air-transmitted infections for surgical site infections (SSIs) after orthopaedic surgery. Research has been hindered by both the inability in blinding the exposure, and by the need for recruiting large enough cohorts. The aim of this study is to investigate whether using a new form of air purifier using plasma air purification (PAP) in operating rooms (ORs) lowers the SSI rate or not. Methods and analysis Multicentre, double-blind, cluster-randomised, placebo-controlled trial conducted at seven hospitals in 2017-2022. All patients that undergo orthopaedic surgery for minimum 30 min are included. Intervention group: patients operated in OR with PAP devices turned on. Control group: patients operated in OR with PAP devices turned off. Randomisation: each OR will be randomised in periods of 4 weeks, 6 weeks or 8 weeks to either have the devices on or off. Primary outcome: any SSI postoperatively defined as a composite endpoint of any of the following: use of isoxazolylpenicillin, clindamycin or rifampicin for 2 days or more, International Classification of Diseases codes or Nordic Medico-Statistical Committee codes indicating postoperative infection. In a second step, we will perform a chart review on those patients with positive indicators of SSI to further validate the outcome. Secondary outcomes are described in the Methods section. Power: we assume an SSI rate of 2%, an SSI reduction rate of 25% and we need approximately 45 000 patients to attain a power of 80% at a significance level of 0.05. Ethics and dissemination The study is approved by the Swedish Ethical Review Authority. The interim analysis results from the study will be presented only to the researchers involved unless the study thereafter is interrupted for whatever reason. Publication in a medical journal will be presented after inclusion of the last patient.

The primary aim of the study was to identify inflammatory markers relevant for osteoarthritis (OA)-related systemic (plasma) and local (synovial fluid, SF) inflammation. From this, we looked for inflammatory markers that coincided with the increased amount of O-linked Tn antigen (GalNAcα1-Ser/Thr) glycan on SF lubricin. Inflammatory markers in plasma and SF in OA patients and controls were measured using a 44-multiplex immunoassay. We found consistently 29 markers detected in both plasma and SF. The difference in their concentration and the low correlation when comparing SF and plasma suggests an independent inflammatory environment in the two biofluids. Only plasma MCP-4 and TARC increased in our patient cohort compared to control plasma. To address the second task, we concluded that plasma markers were irrelevant for a direct connection with SF glycosylation. Hence, we correlated the SF-inflammatory marker concentrations with the level of altered glycosylation of SF-lubricin. We found that the level of SF-IL-8 and SF-MIP-1α and SF-VEGFA in OA patients displayed a positive correlation with the altered lubricin glycosylation. Furthermore, when exposing fibroblast-like synoviocytes from both controls and OA patients to glycovariants of recombinant lubricin, the secretion of IL-8 and MIP-1α and VEGFA were elevated using lubricin with Tn antigens, while lubricin with sialylated and nonsialylated T antigens had less or no measurable effect. These data suggest that truncated glycans of lubricin, as found in OA, promote synovial proinflammatory cytokine production and exacerbate local synovial inflammation.

Osteoarthrithis (OA) is an endemic disease due to the increase of the world’s elderly population. Previously thought to be a consequence of an imbalance between cartilage degradation and biosynthesis, it is now recognized as a disease also involving inflammation, hence influencing the level of inflammatory cytokines, growth factors and chemokines. Lubricin is a mucin type molecule where its OA induced glycosylation truncation propels a deteriorating lubrication of the articular cartilage. The objective of this study was to explore the OA driven truncation of O-linked glycosylation of synovial lubricin and its cross talk with systemic and local (synovial fluid, SF) inflammation. We compared the systemic level of cytokines/chemokine in OA patients’ and controls’ plasma with their local level in SF using a 44 plex screen. The level of 27 cytokines and chemokines was consistently measured in both plasma and SF. The data showed that the levels of cytokines and chemokines in OA plasma display limited correlation to their counterpart in SF. The level of synovial IL-8 and MIP-1α and VEGFA in OA patients, but not their plasma level, where the only cytokines that displayed a significant correlation to the observed lubricin O-linked glycosylation truncation. These cytokines were also shown to be upregulated exposing fibroblast like synoviocytes from healthy and OA patients to recombinant lubricin with truncated glycans mainly consisting of Tn-antigens, while lubricin with sialylated and non-sialylated T anigens did not have any effect. The data suggest that truncated glycans of lubricin, as found in OA, promotes the synovial cytokine production and exerebate the local synovial inflammation.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

The synovial fluid glycoprotein lubricin (also known as proteoglycan 4) is a mucin-type O-linked glycosylated biological lubricant implicated to be involved in osteoarthritis (OA) development. Lubricin's ability to reduce friction is related to its glycosylation consisting of sialylated and unsialylated Tn-antigens and core 1 and core 2 structures. The glycans on lubricin have also been suggested to be involved in crosslinking and stabilization of the lubricating superficial layer of cartilage by mediating interaction between lubricin and galectin-3. However, with the spectrum of glycans being found on lubricin, the glycan candidates involved in this interaction were unknown. Here, we confirm that the core 2 O-linked glycans mediate this lubricin-galectin-3 interaction, shown by surface plasmon resonance data indicating that recombinant lubricin (rhPRG4) devoid of core 2 structures did not bind to recombinant galectin-3. Conversely, transfection of Chinese hamster ovary cells with the core 2 GlcNAc transferase acting on a mucin-type O-glycoprotein displayed increased galectin-3 binding. Both the level of galectin-3 and the galectin-3 interactions with synovial lubricin were found to be decreased in late-stage OA patients, coinciding with an increase in unsialylated core 1 O-glycans (T-antigens) and Tn-antigens. These data suggest a defect in crosslinking of surface-active molecules in OA and provide novel insights into OA molecular pathology.

Patients sustaining a hip fracture have a high mortality rate during the first postoperative year and the Sernbo score may stratify patients into a high, intermediate and low risk of death during this period. We assessed its predictive properties on patients from the National Swedish Hip Fracture Register. 55,716 hip fracture patients, 69% women older than 65 years at surgery (registered between 2010 and 2015) with complete Sernbo scores and mortality data were studied. Receiver-operating characteristics analyses (ROC) were used. Validation of Sernbo score was performed. The overall 1-year mortality rate was 26%—and 17%, 27.4% and 55.6% in the low, intermediate and high-risk groups, respectively. The ROC analysis indicated a predictive ability of the Sernbo score, with an AUC of 0.69 (CI 0.68–0.69). In this registry-based study, the easy-to-use Sernbo scoring system proved to be appropriate and useful way to identify hip fracture patients with a high-risk mortality during the first postoperative year.

Introduction The literature regarding undisplaced femoral neck fractures (FNF) is sparse. The aim of this prospective feasibility study is to compare the clinical outcome after undisplaced FNF treated with internal fixation (IF) and displaced FNF treated with hip arthroplasty. We hypothesized that hip arthroplasty would give a lower incidence of reoperations. Methods A total of 235 patients were included with a median age of 84 years (range 65–99). A consecutive series of 65 patients with undisplaced FNF were treated with IF, and 170 patients with displaced FNF were treated with either a total hip arthroplasty or a hemiarthroplasty. Follow-up interviews were conducted at 1 year using the Harris Hip Score (HHS), WOMAC, and pain numeric rating scale (PNRS). The minimum follow-up time was 22 months. There was no difference in baseline data between the groups. Results Nineteen (8%) hips required reoperation at least once at a mean of 6 months (range 0–35). The rate of reoperation was higher in the IF group compared to the hip arthroplasty group (13.8% vs. 5.9%, 95% CI 0.9–6.4). The overall 1-year and 2-year mortality was 28% and 40%, respectively, with no difference between the groups. The most common reasons for reoperations in the IF group were non-union and avascular necrosis, and 6 patients were treated with hip or excision arthroplasty. In the arthroplasty group, the most common indications were deep infection and dislocation. We did not find any differences between the groups in terms of HHS, WOMAC, and PNRS. Conclusions In this feasibility study, we found no differences in patient-reported outcomes between the groups although IF required a higher rate of reoperations. Further randomized trials are needed to establish the optimal treatment of undisplaced FNF in the elderly. Trial registration ClinicalTrial.org , NCT03392285. Retrospectively registered on 5 February 2018.

Lubricin (PRG4) is a mucin type protein that plays an important role in maintaining normal joint function by providing lubrication and chondroprotection. Improper lubricin modification and degradation has been observed in idiopathic osteoarthritis (OA), while the detailed mechanism still remains unknown. We hypothesized that the protease cathepsin G (CG) may participate in degrading lubricin in synovial fluid (SF). The presence of endogenous CG in SF was confirmed in 16 patients with knee OA. Recombinant human lubricin (rhPRG4) and native lubricin purified from the SF of patients were incubated with exogenous CG and lubricin degradation was monitored using western blot, staining by Coomassie or Periodic Acid-Schiff in gels, and with proteomics. Full length lubricin (∼300 kDa), was efficiently digested with CG generating a 25-kDa protein fragment, originating from the densely glycosylated mucin domain (∼250 kDa). The 25-kDa fragment was present in the SF from OA patients, and the amount was increased after incubation with CG. A CG digest of rhPRG4 revealed 135 peptides and 72 glycopeptides, and confirmed that the protease could cleave in different domains of lubricin. Our results suggest that synovial CG may take part in the degradation of lubricin, which could affect the lubrication of OA joints.

ABSTRACT Synovial fluid lubricin (proteoglycan 4) is a mucin-type O -linked glycosylated (60% of the mass) biological lubricant involved in osteoarthritis (OA) development. Lubricin has been reported to be cross-linked by synovial galectin-3 on the lubricating articular surface. Here, we confirm that binding to galectin-3 depended on core-2 O -linked glycans, where surface plasmon resonance of a recombinant lubricin (rhPRG4) devoid of core-2 structures lacked binding capacity to recombinant galectin-3. Both galectin-3 levels and interactions with synovial lubricin were found to be decreased in late-stage OA patients coinciding with an increase of truncated and less sialylated core 1 O-glycans. These data suggest a defect cross-linking of surface active molecules in OA and provides novel insights into OA molecular pathology.

Background: Pseudotumor formation following total hip arthroplasty (THA) is a well-known complication mainly associated with metal-on-metal (MoM) bearings and taper corrosion on modular-neck femoral stems. The purpose of this study was to determine the prevalence of revision surgery for symptomatic pseudotumors in a large cohort of patients treated with primary THA with a standard stem and a non-MoM articulation. Methods: We included 2,102 patients treated with a total of 2,446 THAs from 1999 until May 2016 in a prospective, observational cohort study. All patients underwent THA with the same uncemented, non-modular-neck femoral stem and metal-on-polyethylene (MoP) (n = 2,409) or ceramic-on-polyethylene (n = 37) articulation. All patients were followed by means of a combination of surgical and medical chart review, follow-up visits, and the Swedish Hip Arthroplasty Register. Metal artifact reduction sequence magnetic resonance imaging (MARS MRI) was used for diagnosis of the pseudotumors, and serum metal ion levels and inflammatory marker levels were measured for all patients who underwent a revision due to pseudotumor. Results: The prevalence of revision for symptomatic pseudotumor formation was 0.5% (13 cases) at a mean follow-up time of 7 years. The incidence rate was 0.9 case per 1,000 person-years. All 13 revisions were done in patients with an MoP articulation. Conclusions: This study demonstrated a 0.5% prevalence of revision due to symptomatic pseudotumor formation in a cohort of patients who underwent THA with a non-MoM construct. Surgeons should be aware that symptomatic pseudotumor formation requiring revision surgery is a tangible complication even after standard MoP THA. Level of Evidence: Therapeutic Level IV. See Instructions for Authors for a complete description of levels of evidence.

Background Patients with surgically treated osteoarthritis of the hip have an increased risk of cardiovascular morbidity and mortality many years after the operation compared with controls. Our hypothesis is that this increased risk after total hip arthroplasty (THA) is mediated by development of periprosthetic osteolysis leading to aseptic loosening of the implant. Methods We conducted a nation-wide, nested, case-control study consisting of patients receiving a cemented THA due to osteoarthritis between the years 1992 and 2005. Our study population included a total of 14,430 subjects identified in the Swedish hip arthroplasty register and linked to the Swedish National Patient Register. The case group consisted of patients (n = 2,886) who underwent reoperation of the treated hip due to osteolysis or aseptic loosening at any time within five years after the index surgery. Each case was matched with four controls (n = 11,544) who had not undergone reoperation. The main outcomes were cardiovascular events i.e. myocardial infarction, heart failure and cerebral infarction according to ICD-codes and time to the first cardiovascular event during the exposure period. Outcomes were subgrouped into cardiac and cerebral events. We used regression models to calculate the incidence rates and adjusted our results for confounders. Findings Overall, 5.1% of patients had cardiac events, with slightly more overall cardiovascular events occurring in the control group (8.1% vs. 6.7%, odds ratio 0.8, 95% confidence interval (CI) 0.7 to 1.0). After adjusting for confounders, the case group had an increased relative risk of 1.3 (95% confidence interval (CI) 1.1 to 1.3) for total number of cardiovascular events. Similar effect sizes were observed for time to first event. Interpretation Patients with osteoarthritis who received THA and subsequently underwent a revision operation due to loosening had a higher relative risk of developing cardiovascular events than controls. Thus there is an association which could be explained by a common inflammatory disease pathway that requires further experimental research.

Background: Periprosthetic osteolysis by polyethylene wear debrisetriggered osteoclasts is viewed as the main pathophysiological pathway in aseptic loosening in total hip arthroplasty. The present aim was to study osteoclast occurrence in osteolytic lesions in early and late revisions of the Charnley low-friction torque arthroplasty (CLFA). Methods: Biopsies of the soft interface membrane and the adjacent bone were taken from osteolytic lesions during revision of 16 loose CLFA, early (2-6 years) or late (> 10 years) after primary surgery. By light microscopy (LM), cell-dense regions with signs of osteoclast-mediated bone resorption were selected for transmission electron microscopy. Three additional patients were studied in LM for osteoclast markers (tartrate-resistant acid phosphatase and Cathepsin K). Results: LM disclosed a low-grade chronic inflammation and birefringent particles in most sections. Multiple conglomerates of tartrate-resistant acid phosphatase positive and Cathepsin K positive mononuclear and multinucleated cells were found deep in the fibrous interface membrane. Transmission electron microscopy showed traces of polyethylene-like particles in 67%-100% of the cells. Osteoclast-like cells exhibiting resorptive activity were few (mean, 0.7%; standard deviation, 0.2%), and multinucleated cells, possibly osteoclast precursor cells, located immediately on the bone were also scarce (mean, 2.7%; standard deviation, 5.3%). Multinucleated (odds ratio, 3.0; 95% confidence interval, 1.7-5.5) and macrophage-like cells (odds ratio, 3.6; 95% confidence interval, 2.2-5.6) were typically located deeper in the inflammatory interface membrane with a pathologic appearance with distension and abundance of phagocytic vacuoles. There were no systematic differences in cell populations between early or late revisions. Conclusion: Despite probable ongoing osteoclastogenesis in the osteolytic lesions, there were few sites of osteoclast-mediated bone resorption. These findings attach a contributing biological explanation to the longevity of the CLFA. (C) 2017 Elsevier Inc. All rights reserved.

Lubricin, a heavily O -glycosylated protein, is essential for boundary lubrication of articular cartilage. Strong surface adherence of lubricin is required given the extreme force it must withstand. Disulfide bound complexes of lubricin and cartilage oligomeric matrix protein (COMP) have recently been identified in arthritic synovial fluid suggesting they may be lost from the cartilage surface in osteoarthritis and inflammatory arthritis. This investigation was undertaken to localise COMP-lubricin complexes within cartilage and investigate if other cartilage proteins are involved in anchoring lubricin to the joint. Immunohistochemical analysis of human cartilage biopsies showed lubricin and COMP co-localise to the cartilage surface. COMP knockout mice, however, presented with a lubricin layer on the articular cartilage leading to the further investigation of additional lubricin binding mechanisms. Proximity ligation assays (PLA) on human cartilage biopsies was used to localise additional lubricin binding partners and demonstrated that lubricin bound COMP, but also fibronectin and collagen II on the cartilage surface. Fibronectin and collagen II binding to lubricin was confirmed and characterised by solid phase binding assays with recombinant lubricin fragments. Overall, COMP, fibronectin and collagen II bind lubricin, exposed on the articular cartilage surface suggesting they may be involved in maintaining essential boundary lubrication.

Purpose: The purpose of this study was to investigate and explore nurse's previous experiences of patient care in MBRs before their further education in anesthesia. Design: Qualitative research. Methods: Data were collected through three focus group interviews using content data analysis. Findings: Maintaining patient privacy, providing conditions for communication between health care professionals and patients, and undertaking daily practical care were stated as the main problems in MBR care. Inferior conditions for providing sensitive information and communication with proxies, especially in association with language problems, were frequently encountered. Patient's proxies could facilitate several problematic issues in MBR care. Conclusions: The present study characterized well-defined and easily recognizable clinical problems experienced in the care of patients in an MBR setting from a nurse's perspective. The opinion shared by most nurses was that the inability to implement privacy, dignity, and sound communication with patients should be taken into account in future hospital designs. General dissatisfaction with work environment, increased stress, and the risk of errors in care may otherwise follow.

Background and purpose — Displaced femoral neck fractures (FNFs) are associated with high rates of mortality during the first postoperative year. The Sernbo score (based on age, habitat, mobility, and mental state) can be used to stratify patients into groups with different 1-year mortality. We assessed this predictive ability in patients with a displaced FNF treated with a hemiarthroplasty or a total hip arthroplasty. Patients and methods — 292 patients (median age 83 (65–99) years, 68% female) with a displaced FNF were included in this prospective cohort study. To predict 1-year mortality, we used a multivariate logistic regression analysis including comorbidities and perioperative management. A receiver operating characteristic (ROC) analysis was used to evaluate the predictive ability of the Sernbo score, which was subsequently divided in a new manner into a low, intermediate, or high risk of death during the first year. Results — At 1-year follow-up, the overall mortality rate was 24%, and in Sernbo’s low-, intermediate-, and high-risk groups it was 5%, 22%, and 51%, respectively. The Sernbo score was the only statistically significant predictor of 1-year mortality: odds ratio for the intermediate-risk group was 4.2 (95% Cl: 1.5–12) and for the high-risk group it was 15 (95% CI: 5–40). The ROC analysis showed a fair predictive ability of the Sernbo score, with an area under the curve (AUC) of 0.79 (95% CI: 0.73–0.83). Using a cutoff of less than 11 points on the score gave a sensitivity of 61% and a specificity of 83%. Interpretation — The Sernbo score identifies patients who are at high risk of dying in the first postoperative year. This scoring system could be used to better tailor perioperative care and treatment in patients with displaced FNF.