Update This article was updated on September 4, 2020, because of a previous error. On page 1211, in the author affiliation section, “W.L. Walter, MBBS, PhD3” now reads “W.L. Walter, MBBS, PhD3,4,” the affiliation for Dr. Van Onsem that had read “3Specialist Orthopedic Group, The Mater Clinic, North Sydney, New South Wales, Australia” now reads “3Royal North Shore Hospital, St. Leonards, New South Wales, Australia,” and the affiliation for Dr. Walter that had read “3Specialist Orthopedic Group, The Mater Clinic, North Sydney, New South Wales, Australia” now reads “3Royal North Shore Hospital, St. Leonards, New South Wales, Australia” and “4University of Sydney, Sydney, New South Wales, Australia.” An erratum has been published: J Bone Joint Surg Am. 2020 Oct 7;102(19):e113 » As we resume elective surgical procedures, it is important to understand what practices and protocols should be altered or implemented in order to minimize the risk of pathogen transfer during the severe acute respiratory syndrome (SARS)-CoV-2 pandemic.» Each hospital and health system should consider their unique situation in terms of SARS-CoV-2 prevalence, staffing capabilities, personal protection equipment supply, and so on when determining how and when to implement these recommendations.» All patients should be screened for SARS-CoV-2 by means of a thorough history and physical examination, as well as reverse transcription-polymerase chain reaction (RT-PCR) testing whenever possible, prior to undergoing elective surgery.» Patients who are currently infected with coronavirus disease 2019 (COVID-19) should not undergo elective surgery.» These guidelines are based on the available scientific evidence, albeit scant. The recommendations have been reviewed and voted on by the expert delegates who produced this document.

BackgroundAlso known as clubfoot, idiopathic congenital talipes equinovarus (ICTEV) is the most common pediatric deformity and occurs in 1 in every 1000 live births. Even though it has been widely researched, the etiology of ICTEV remains poorly understood and is often described as being based on a multifactorial genesis. Genetic and environmental factors seem to have a major role in the development of this disease. Thus, the aim of this review is to analyze the available literature to document the current evidence on ICTEV etiology.MethodsThe literature on ICTEV etiology was systematically reviewed using the following inclusion criteria: studies of any level of evidence, reporting clinical or preclinical results, published in the last 20 years (1998–2018), and dealing with the etiology of ICTEV.ResultsA total of 48 articles were included. ICTEV etiology is still controversial. Several hypotheses have been researched, but none of them are decisive. Emerging evidence suggests a role of several pathways and gene families associated with limb development (HOX family; PITX1-TBX4), the apoptotic pathway (caspases), and muscle contractile protein (troponin and tropomyosin), but a major candidate gene has still not been identified. Strong recent evidence emerging from twin studies confirmed major roles of genetics and the environment in the disease pathogenesis.ConclusionsThe available literature on the etiology of ICTEV presents major limitations in terms of great heterogeneity and a lack of high-profile studies. Although many studies focus on the genetic background of the disease, there is lack of consensus on one or multiple targets. Genetics and smoking seem to be strongly associated with ICTEV etiology, but more studies are needed to understand the complex and multifactorial genesis of this common congenital lower-limb disease.

Introduction Osteoarthritis (OA) is a degenerative joint disease characterized by articular cartilage degradation, subchondral damage, and bone remodelling, affecting most commonly weight-bearing joints, such as the knee and hip. The loss of cartilage leads to joint space narrowing, pain, and loss of function which could ultimately require total joint replacement. The Wnt/β catenin pathway is involved in the pathophysiology of OA and has been proposed as a therapeutic target. Endogenous and pharmacological inhibitors of this pathway were recently investigated within innovative therapies including the use of platelet-rich plasma (PRP) and mesenchymal stem cells (MSCs). Methods A review of the literature was performed on the PubMed database based on the following inclusion criteria: article written in English language in the last 20 years and dealing with (1) the role of Wnt-β catenin pathway in the pathogenesis of osteoarthritis and (2) pharmacologic or biologic strategies modulating the Wnt-β catenin pathway in the OA setting. Results Evidences support that Wnt signalling pathway is likely linked to OA progression and severity. Its inhibition through natural antagonists and new synthetic or biological drugs shares the potential to improve the clinical condition of the patients by affecting the pathological activity of Wnt/β-catenin signalling. Conclusions While further research is needed to better understand the mechanisms regulating the molecular interaction between OA regenerative therapies and Wnt, it seems that biologic therapies for OA exert modulation on Wnt/β catenin pathway that might be relevant in achieving the beneficial clinical effect of those therapeutic strategies.

Background Inflammation and mechanical demands play a role in the development of tendon conditions and the dysregulation of tendon healing. In patients with obesity, high levels of pro-inflammatory cytokines and a high mechanical demand promote chronic low-grade inflammation. Although controversial results have been reported, we aimed to summarize current evidence while highlighting the role of obesity in tendinopathy. Questions/purposes (1) Do patients with obesity have a greater risk of tendinopathy, stratified by upper and lower extremity sites, than patients who do not have obesity? (2) Is obesity associated with a higher risk of upper and lower extremity tendon tear and ruptures? (3) Is obesity associated with an increased risk of complications after upper and lower extremity tendon surgery? Methods We performed a systematic review by searching the PubMed, Embase, and Cochrane Library databases, combining the term “tendon” with common terms for tendinopathy and rupture such as “tendon injury OR tendinopathy OR tendon rupture” and “obese” OR “obesity.” We included studies with any level of evidence published from January 2000 to July 10, 2019 in peer-reviewed journals reporting clinical results. After we removed the duplicates, there were 365 records. Two independent authors screened these records and excluded 320 based on abstract and title screening. Of the remaining 45 studies, 23 were excluded because the topic did not address the research questions (n = 19), the article was outdated (n = 3), or because there was a serious risk of bias (n = 1). Finally, we included 22 studies with 49,914 participants (5984 with obesity), 31,100 (1884 with obesity) of whom had upper-extremity tendinopathy, while 18,814 (4010 with obesity) had lower-extremity tendinopathy. Obesity was defined as a BMI ≥ 30 kg/m2 according to the WHO’s criteria. Data were extracted and analyzed critically. Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines were applied, and the risk of bias (ROBINS tool) of the studies was assessed, as was the methodological quality (Coleman score). The assessment was performed independently by two authors. Inter-rater agreement for the assessments of the risk of bias and methodological quality were 89% and 94%, respectively. All studies were observational, and most were retrospective case-control studies. Any discrepancy was discussed and solved by consensus. The articles had a moderate risk of bias (eight articles) or a low risk of bias (fourteen articles). We excluded one article because of a serious risk of bias. The mean (range) Coleman score was 53.5 (42-74). Results Obesity was associated with a greater risk of upper extremity tendinopathy (rotator cuff: odds ratio 1.25 [95% confidence interval 1.12 to 1.40]; p < 0.001; medial epicondylitis: OR 1.9 [95% CI 1.0 to 3.7]; p < 0.05) and lower-extremity tendinopathy (Achilles tendon: OR 3.81 [95% CI 2.57 to 5.63]; OR 3.77 [95% CI 2.24 to 6.34]; OR 6.56 [95% CI 3.18 to 13.55], for obesity Classes I, II and III, respectively; patellar tendon: OR 1.10 [95% CI 1.05 to 1.90]; p = 0.001; plantar fascia: OR 2.97 [95% CI 1.64 to 5.37]; p = 0.004). Obesity was associated with a greater risk of upper extremity tendon tear (rotator cuff: OR 2.35 [95% CI 1.62 to 3.40]; p < 0.001) and rupture leading to tendon surgery (rotator cuff in men: OR 3.13 [95% CI 1.29 to 7.61]; p < 0.001 and women: OR 3.51 [95% CI 1.80 to 6.85]; p < 0.001). However, no association was found between BMI and lower extremity rupture (Achilles mean BMI: 27.77 kg/m2 [95% CI 26.94 to 28.49] versus control: 26.66 kg/m2 [95% CI 26.06 to 27.27]; p = 0.047). Upper extremity complications (n = 359) after tendon repair surgery had a weighted incidence of 13.27% and 8.13% for rotator cuff surgery in patients with and without obesity, respectively. In the lower extremity (n = 21,152), the weighted incidence for Achilles tendon surgery was 11.28% and 8.6% in patients with and without obesity, respectively. Conclusions Obesity is associated with a higher risk of tendinopathy, tendon tear and rupture, and complications after tendon surgery than non-obesity. However, the high heterogeneity and observational nature of the studies highlight the need to be cautious about the results of our study. We encourage researchers to perform clinical and preclinical studies to explore pathways related to the metabolic state of this population. Level of Evidence Level IV, prognostic study.

Background: A large body of evidence is emerging to implicate that dysregulation of the gut microbiome (dysbiosis) increases the risk of surgical site infections. Gut dysbiosis is known to occur in patients with inflammatory bowel disease (IBD), allowing for translocation of bacteria across the inflamed and highly permeable intestinal mucosal wall. The null hypothesis was that IBD was not associated with an increased risk of periprosthetic joint infection (PJI) after primary total hip and knee arthroplasty.Methods: A matched cohort study was designed. The primary end point was the occurrence of PJI at 2 years postoperatively. The secondary end points were aseptic revisions at 2 years postoperatively, discharge to a rehabilitation facility, complications up to 30 days after total joint arthroplasty, and readmission up to 90 days after total joint arthroplasty. The International Classification of Diseases, Ninth Revision (ICD-9) and Tenth Revision (ICD-10) codes were used to identify patients with IBD and the control cohort. A chart review was performed to confirm the diagnosis of IBD. Using our institutional database, 152 patients with IBD were identified and matched (3:1) for age, sex, body mass index, year of surgical procedure, Charlson Comorbidity Index, and involved joint with 456 patients without IBD undergoing total joint arthroplasty. Results:The cumulative incidence of PJI was 4.61% for the patients with IBD compared with 0.88% for the control cohort (p = 0.0024). When univariable Cox regression was performed, a diagnosis of IBD was found to be an independent risk factor for PJI (hazard ratio [HR], 5.44 [95% confidence interval (CI), 1.59 to 18.60]; p = 0.007) and aseptic revisions (HR, 4.02 [95% CI, 1.50 to 10.79]; p = 0.006). The rate of postoperative complications was also higher in patients with IBD.Conclusions: Based on the findings of this study, it appears that patients with IBD are at higher risk for treatment failure due to PJI or aseptic loosening after primary total joint arthroplasty. The exact reason for this finding is not known, but could be related to bacterial translocation from the inflamed intestinal mucosa, the dysregulated inflammatory status of these patients, malnutrition, and potentially other factors. Some of the aseptic failures could be as a result of infection that may have escaped detection and/or recognition.

Background Tendinopathy is a common musculoskeletal condition affecting subjects regardless of their activity level. Multiple inflammatory molecules found in ex vivo samples of human tendons are related to the initiation or progression of tendinopathy. Their role in tendon healing is the subject of this review. Sources of data An extensive review of current literature was conducted using PubMed, Embase and Cochrane Library using the term ‘tendon’, as well as some common terms of tendon conditions such as ‘tendon injury OR (tendon damage) OR tendonitis OR tendinopathy OR (chronic tendonitis) OR tendinosis OR (chronic tendinopathy) OR enthesitis’ AND ‘healing’ AND ‘(inflammation OR immune response)’ as either key words or MeSH terms. Areas of agreement An environment characterized by a low level of chronic inflammation, together with increased expression of inflammatory cytokines and growth factors, may influence the physiological tendon healing response after treatment. Areas of controversy Most studies on this topic exhibited limited scientific translational value because of their heterogeneity. The evidence associated with preclinical studies is limited. Growing points The role of inflammation in tendon healing is still unclear, though it seems to affect the overall outcome. A thorough understanding of the biochemical mediators of healing and their pathway of pain could be used to target tendinopathy and possibly guide its management. Areas timely for developing research We require further studies with improved designs to effectively evaluate the pathogenesis and progression of tendinopathy to identify cellular and molecular targets to improve outcomes.

BACKGROUNDLegg-Calvé-Perthes disease (LCPD) is a clinical condition affecting the femoral head of children during their growth. Its prevalence is set to be between 0.4/100000 to 29.0/100000 children less than 15 years of age with a peak of incidence in children aged from 4 years to 8 years. LCPD aetiology has been widely studied, but it is still poorly understood.AIMTo analyse the available literature to document the up-to-date evidence on LCPD aetiology.METHODSA systematic review of the literature was performed regarding LCPD aetiology, using the following inclusion criteria: studies of any level of evidence, reporting clinical or preclinical results and dealing with the aetiology or pathogenesis of LCPD. Two reviewers searched the PubMed and Science Direct databases from their date of inception to the 20th of May 2018 in accordance with the Preferred Reporting Items for Systemic Reviews and Meta-Analyses guidelines. To achieve the maximum sensitivity of the search strategy, we combined the terms: ‘‘Perthes disease OR LCPD OR children avascular femoral head necrosis” with “pathology OR aetiology OR biomechanics OR genetics” as either key words or MeSH terms.RESULTSWe include 64 articles in this review. The available evidence on LCPD aetiology is still debated. Several hypotheses have been researched, but none of them was found decisive. While emerging evidence showed the role of environmental risk factors and evidence from twin studies did not support a major role for genetic factors, a congenital or acquired predisposition cannot be excluded in disease pathogenesis. One of the most supported theories involved mechanical induced ischemia that evolved into avascular necrosis of the femoral head in sensible patients.CONCLUSIONThe literature available on the aetiology of LCPD presents major limitations in terms of great heterogeneity and a lack of high-profile studies. Although a lot of studies focused on the genetic, biomechanical and radiological background of the disease, there is a lack of consensus on one or multiple major actors of the etiopathogenesis. More studies are needed to understand the complex and multifactorial genesis of the avascular necrosis characterizing the disease.

Periprosthetic joint infection in total knee arthroplasty is a significant complication that is a common reason for revision surgery. The current standard of care is two-stage revision surgery. There is however increasing evidence to support the use of single-stage revision surgery. We conducted a PRISMA systematic review of the current evidence on the use of single-stage revision for infected total knee arthroplasty. Four databases (PubMed, Embase, Science Direct, and Cochrane Library) were systematically screened for eligible studies. The risk bias of each study was identified using ROBINS-I tool, and the quality of evidence was assessed using the GRADE criteria. Sixteen articles were retained after applying the inclusion and exclusion criteria that evaluated 3645 knee single-stage revision surgeries. Our review reveals satisfactory outcomes for single-stage revision in the management of infected total knee arthroplasty. The reinfection rates in the studies included in our review varied however the majority reported low reinfection rates and good functional outcomes. Although strict patient selection criteria have yielded successful results, good results were also reported when these criteria were not applied. The greater use of risk factors in identifying patients likely to have a successful outcome needs to be balanced with the practical benefits of performing a single stage procedure in higher risk patients. Future large clinical randomized control trials are required to confirm our results.