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Background Reporting of complications after total hip arthroplasty (THA) is not standardized, and it is done inconsistently across various studies on the topic. Advantages of standardizing complications include improved patient safety and outcomes and better reporting in comparative studies. Questions/purposes The purpose of this project was to develop a standardized list of complications and adverse events associated with THA, develop standardized definitions for each complication, and stratify the complications.

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Background: Changes in the joint microenvironment after an injury to the articular surface of the knee have been implicated in the pathogenesis of osteoarthritis. While prior studies focused on changes in this microenvironment after anterior cruciate ligament ruptures, few have explored the biomarker changes that occur in the setting of meniscal injuries. Purpose: To determine whether meniscal injury results in significant alterations to synovial fluid biomarker concentrations as compared with noninjured contralateral knees. Additionally, to explore the relationship between synovial fluid biomarkers and the degree of cartilage injury seen in these patients. Study Design: Cross-sectional study; Level of evidence, 3. Methods: Patients undergoing surgery for unilateral meniscal injury were prospectively enrolled from October 2011 to December 2016, forming a cohort that had synovial fluid samples collected from both the injured knee and the contralateral uninjured knee at the time of meniscal surgery. Synovial fluid samples were collected just before incision, and the concentrations of 10 biomarkers of interest were determined with a multiplex magnetic bead immunoassay. The concentrations of synovial fluid biomarkers from the operative and contralateral knees were compared. Additionally, the synovial fluid biomarker concentrations of operative knees from patients with associated high-grade cartilage lesions were compared with those with low-grade lesions. Results: The current analysis included synovial fluid samples from 82 knees (41 operative and 41 contralateral) from 41 patients undergoing arthroscopic surgery to treat a symptomatic meniscal injury. The mean ± SD age of patients was 49.86 ± 11.75 years. There were significantly greater concentrations of 4 of the 5 proinflammatory biomarkers (IL-6, MCP-1, MIP-1β, and MMP-3) in symptomatic knees as compared with asymptomatic knees when controlling for the duration of symptoms, body mass index, age, and the random effects of by-patient variability. In the injured knees, associated high-grade cartilage lesions were predictive of elevated MCP-1, MIP-1β, and VEGF levels. Low synovial fluid concentration of TIMP-1 or a greater ratio of MMP-3 to TIMP-1 was associated with the presence of synovitis. Increasing age was found to be an independent predictor of increased IL-6, MCP-1, and VEGF concentrations in the setting of symptomatic meniscal injury. Conclusion: The authors identified 4 proinflammatory synovial fluid biomarkers whose concentrations were significantly different after meniscal injury as compared with uninjured contralateral knees. Furthermore, they describe the effects of associated cartilage damage, synovitis, and patient age on biomarker concentrations.

Introduction Signal transducers and activators of transcription (STAT) proteins are transcription factors that when activated, by phosphorylation, regulate gene expression and cellular activity. The aim of this study was to evaluate the local and systemic expression and activation of STAT proteins associated with abdominal aortic aneurysms (AAA). Methods Expression and activation of STAT proteins were assessed in aortic wall samples obtained from patients undergoing repair of AAA (N=9) and from non-aneurysmal (NA) donors (N=17). Aortic samples were evaluated for mRNA and protein expression for STAT1, 2, 3, 4, 5a, and 5b using RT-PCR and immunoblot (WB) assays and normalized to β-actin (expressed as arbitrary units). STAT activation was assessed with WB assays using phosphorylated (p)-STAT-specific antibodies. Alterations in STAT activation were calculated by normalizing p-STAT proteins to corresponding total STAT levels. Immunohistochemistry was performed on AAA and NA samples using the total and pSTAT antibodies.Systemic alterations in STAT activation were assessed by evaluating circulating leukocytes for the presence of p-STAT from patients with AAA (AAA, N=8), repaired aneurysm (RA, N=8), or age/gender matched controls with no AAA (CT, N=8). Flow cytometry was performed to assess for circulating levels of STAT1 (pY701), STAT3 (pY705), and STAT5a (pY694) in monocytes, granulocytes, and lymphocytes. Assessments were made at baseline and in response to in vitro stimulation with IFN-gamma (50 ng/mL) or IL-6 (100 ng/mL). Results were analyzed using Student’s T-test and are expressed as mean±SEM. Results In AAA tissue compared to NA, STAT-1 (1.08±0.09 v. 0.62±0.07), -2 (0.98±0.07 v. 0.55±0.08), and -4 (0.89±0.12 v. 0.35±0.11) mRNA levels were elevated (P<0.01, all). Corresponding increases in STAT protein were only observed for STAT1 (2.77±0.93 v. 0.93±0.08, P<0.05). Increases in activation were observed in AAA compared to NA in p-STAT2 (0.77±0.1 v. 0.1±0.02, P<0.01), p-STAT3 (1.6±0.3 v. 0.2±0.06, P<0.02) and p-STAT5 (0.57±0.03 v. 0.2±0.03, P<0.05) levels. Phosphorylated STAT1, 2, 3, and 5 were observed in inflammatory cells invading the AAA adventitia. In addition, STAT3 was observed in the media of AAA and NA, but pSTAT3 was only observed in the media of AAA. There were no differences in baseline levels of p-STAT-positive circulating leukocytes. IFN-gamma stimulation decreased STAT-5a (pY694)-positive CT lymphocytes to 40±13% of baseline, but had no effect on AAA or RA lymphocytes (116±35%, 102±19%, respectively; P=0.01). STAT-5a (pY694)-positive CT granulocytes also decreased to 62±18% of baseline compared to AAA or RA granulocytes (122±25%, 126±17%, respectively; P=0.01). Alterations in STAT1 (pY701) and STAT3 (pY705) were not observed in leukocytes following cytokine stimulation. Conclusions STAT proteins are important regulators of transcriptional activity and have been linked to cardiovascular disease. The present data suggest that altered levels of phosphorylated STATs are associated with AAA. Unders...

Bone loss often complicates revision total knee arthroplasty (TKA). Management of metaphyseal defects varies, with no clearly superior technique. Two commonly utilized options for metaphyseal defect management include porous-coated metaphyseal sleeves and tantalum cones. A systematic review was conducted according to the international Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We combined search terms “Total knee arthroplasty” AND/OR “Sleeve,” “Cone” as either keywords or medical subject heading (MeSH) terms in multiple databases according to PRISMA recommendations. All retrieved articles were reviewed and assessed using defined inclusion and exclusion criteria. A total of 27 studies (12 sleeves and 15 cones) of revision TKAs were included. In the 12 studies on sleeve implantation in revision TKAs, 1,617 sleeves were implanted in 1,133 revision TKAs in 1,025 patients. The overall rate of reoperation was 110/1,133 (9.7%) and the total rate of aseptic loosening per sleeve was 13/1,617 (0.8%). In the 15 studies on tantalum cone implantation in revision TKAs, 701 cones were implanted into 620 revision TKAs in 612 patients. The overall rate of reoperation was 116/620 (18.7%), and the overall rate of aseptic loosening per cone was 12/701 (1.7%). Rates of aseptic loosening of the two implants were found to be similar, while the rate of reoperation was nearly double in revision TKAs utilizing tantalum cones. Variability in the selected studies and the likely multifactorial nature of failure do not allow for any definitive conclusions to be made. This review elucidates the necessity for additional literature examining revision TKA implants.

Background: Changes in the intra-articular inflammatory state during the immediate period after an acute anterior cruciate ligament (ACL) rupture are not well defined. Purpose: To evaluate changes in the concentration of select proinflammatory and anti-inflammatory synovial fluid cytokines during the interval between an ACL injury and surgical reconstruction. Study Design: Descriptive laboratory study. Methods: In patients with an acute ACL injury, a synovial fluid sample was obtained from the injured knee during the initial office visit within 2 weeks of the inciting traumatic event. An additional synovial fluid sample was collected at the time of ACL reconstruction just before the surgical incision. Synovial fluid samples from both the acute injury and the surgery time points were processed with a protease inhibitor, and the concentrations of 10 cytokines of interest were measured using a multiplex magnetic bead immunoassay. The primary outcome was the change in cytokine concentrations between time points. Results: A total of 20 patients with a mean age of 30.2 ± 8.3 years were included. The acute injury synovial fluid samples were collected at 6.6 ± 3.8 days after the injury. The surgical synovial fluid samples were collected at 31.6 ± 15.6 days after the acute injury samples. Based on a series of linear mixed-effects models to control for the effect of concomitant meniscal injuries and by-patient variability, there was a statistically significant increase in the concentrations of RANTES and bFGF and a statistically significant decrease in the concentrations of IL-6, MCP-1, MIP-1β, TIMP-1, IL-1Ra, and VEGF between time points. Conclusion: This study demonstrates the ongoing alterations in the intra-articular microenvironment during the initial inflammatory response in the acute postinjury period. We identified 6 synovial fluid cytokines that significantly decreased and 2 that significantly increased between the first clinical presentation shortly after the injury and the time of surgery 1 month later. Clinical Relevance: This study describes the molecular profile of the inflammatory changes between the time of an acute ACL injury and the time of surgical reconstruction 1 month later. A greater understanding of the acute inflammatory response within the knee may be helpful in identifying the optimal timing for a surgical intervention that balances the risk of chondral damage with the likelihood of successful, well-healed reconstruction.