Department of Orthopaedic Surgery

ABSTRACT Why do women remain underrepresented in positions of power? The present work leverages four studies ( N = 99,293) spanning archival, qualitative, and experimental methods to surface one novel antecedent to this gender gap. Men (vs. women) tend to perceive their organizations as more meritocratic as a function of their structural power (Studies 1–2). This gender difference is statistically accounted for by the fact that men's power is more often accompanied by perceived resource sufficiency , or the appraisal that one has adequate instrumental and material resources to meet role demands and exercise authority effectively (Studies 1–3). A preregistered experiment finds that higher (vs. lower) perceived resource sufficiency increases meritocracy perceptions, which in turn increase career investment intentions but weaken support for equity‐enhancing initiatives (Study 4). Together, these findings reveal that structural power's psychological consequences are not uniform across gender but depend on whether authority is accompanied by the resources needed to exercise power. The gender gap in power may thus reproduce itself, as women become less convinced that the system rewards their effort, whereas men with the authority to change organizational systems become least likely to see the need for change.

Background Osteoporosis is a well-established risk factor for early femoral failure following cementless total hip arthroplasty (THA). The performance of cementless collared triple-taper stems (CTTSs) in patients with a confirmed diagnosis of osteoporosis remains poorly defined. This study aimed to evaluate early clinico-radiographic outcomes of CTTS in osteoporotic patients undergoing elective THA. Methods We retrospectively reviewed 96 patients (87.5% women; mean age 69.5 ± 7.4 years) who underwent elective THA with a CTTS between 2018 and 2025. Osteoporosis was confirmed by either dual-energy x-ray absorptiometry T-score ≤ −2.5 or history of fragility fracture. Preoperative morphology and postoperative canal fill ratios, alignment, and subsidence (>3 mm) were assessed. Femoral failure was defined as periprosthetic fracture or aseptic loosening. Results Preoperative morphology demonstrated a predominance of wide canals (Dorr B: 67.5%, Dorr C: 26%) and a mean morphological cortical index of 2.55. Postoperatively, high mean canal fill ratios were achieved (Z1: 0.66; Z2: 0.79; Z3: 0.76; Z4: 0.74), indicating reliable metaphyseal and diaphyseal fit. Despite osteoporotic bone quality, no cases of measurable subsidence were observed. Prominent collars occurred in 34.4% and neocortex formation in 5.2%, with no associated complications. At a mean follow-up of 2 years (range 1–7), the primary outcome of femoral failure was 0% at 90 days, 1 year, and final follow-up. Conclusions Cementless CTTS demonstrated reliable early fixation with no femoral failures in a rigorously defined osteoporotic cohort. These findings suggest that cementless CTTS may be a viable option for femoral fixation in osteoporotic patients undergoing elective THA. Level of Evidence Level III, Therapeutic study.

BACKGROUND: Developmental control of jaw size is crucial to prevent birth defects and facilitate evolutionary adaptation. We have shown that jaw size is established by neural crest mesenchyme (NCM), which are progenitor cells that migrate into the mandibular primordia and produce the jaws. NCM relies on multiple signaling pathways including Sonic Hedgehog (SHH) to mediate interactions with mandibular epithelium and promote jaw outgrowth. We investigated if NCM-mediated regulation of the SHH pathway underlies species-specific evolution of jaw size. RESULTS: We analyze expression of SHH pathway members over time and find that Growth Arrest-Specific 1 (GAS1), which is a SHH co-receptor, is expressed 20-75-fold higher in mandibular primordia of duck relative to those of quail. We generate quail-duck chimeras and demonstrate Gas1 expression is NCM-regulated. Gain- and loss-of-function experiments reveal species-specific sensitivity to SHH signaling, especially for Gas1. Gas1 overexpression and knockdown in NCM alters cell number and jaw size, and differentially affects genes involved in the SHH and WNT pathways, the cell cycle, and others. We also uncover intriguing differences in the Gas1 promoter and coding sequence between duck and quail. CONCLUSIONS: Our work suggests changes to Gas1 expression and function may modulate jaw size during development, disease, and evolution.

While gender and economic outcomes in negotiation have been studied for decades, much less is known about gender differences in subjective outcomes, such as trust, rapport, and willingness to negotiate again, despite their importance for long-term success. In a series of studies with over 2,000 participants, we find that people consistently report better subjective outcomes when negotiating with women. This preference persists even in anonymous negotiations where gender is unknown and cannot be inferred from behavior, as well as in conditions where negotiation partner gender is randomly assigned. Importantly, we find no gender difference in economic outcomes. To understand why, we analyzed transcripts of real negotiations for any behavioral differences. These findings reveal an overlooked gender dynamic: While men and women achieve similar economic results, women foster stronger interpersonal relationships, which in turn lead to greater satisfaction and greater desire for future negotiations with women.

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Despite decades of progress, gender inequalities in workplace authority and compensation persist. This review reveals recent advances in understanding how gendered careers emerge through three psychological mechanisms prevalent in organizations: (i) intrapersonal gender biases, (ii) interpersonal power dynamics, and (iii) intergroup gender relations. Because power is perceived as masculine, women in authority face systematic backlash. While status offers women an alternative leadership route, it proves less valuable than power - lacking resource control and requiring constant social validation rather than conferring formal authority. We suggest that mindsets about human malleability moderate these dynamics: fixed mindsets amplify stereotyping and power-based challenges for women leaders, while growth mindsets attenuate barriers. Our framework aims to illuminate gender disparities and to suggest promising intervention pathways.

Background: The European Bone and Joint Infection Society (EBJIS)/Musculoskeletal Infection Society (MSIS) criteria provide a framework for diagnosing hip periprosthetic joint infection, yet daily clinical application lacks a standardized algorithm. Since these criteria rely heavily on synovial fluid markers, surgeons encounter 2 primary dilemmas: the reliability of aspiration techniques (ultrasound vs fluoroscopy) and the economic trade-off between higher-cost proprietary assays and standard institutional laboratories. This cost-effectiveness analysis was conducted to identify the diagnostic pathway that maximizes clinical benefit while minimizing expenditure within the EBJIS/MSIS framework. Methods: A decision tree model simulated the diagnostic workup of a 67-year-old patient with suspected hip periprosthetic joint infection. Ten strategies were evaluated, comparing aspiration modality and laboratory method (institutional, point-of-care, and third-party analysis). The model incorporated 1- and 2-stage revision pathways and included dry tap scenarios. Accuracy inputs were derived from the literature, and costs reflected 2025 Medicare schedules. Sensitivity analyses tested robustness across diagnostic outcomes. Effectiveness was measured in quality-adjusted life years based on downstream surgical outcomes. Results: Ultrasound-guided aspiration with third-party synovial analysis was most cost-effective in both revision scenarios. Despite higher upfront costs of specialized testing, its superior sensitivity and specificity maximized quality-adjusted life years by reducing morbidity from misdiagnosis. Institutional testing was preferred only if sensitivity exceeded 90% and specificity 94%. In "dry tap" cases, intraoperative lateral flow alpha-defensin testing was favored over preoperative nuclear imaging. Surgical outcome utility most strongly influenced the results. Conclusions: Within the EBJIS/MSIS framework, prioritizing high-accuracy diagnostic tools maximizes value by reducing misaligned revision strategies. Diagnostic precision outweighed individual test cost in determining cost-effectiveness. Level of Evidence: Economic and decision analysis, Level II.

Muscle fibrosis is a key pathological feature of Duchenne muscular dystrophy (DMD) and is closely associated with disease progression. Fibroadipogenic progenitors (FAPs) are major contributors to fibrosis, yet the precise mechanisms remain unclear. To investigate FAP dynamics and lineage specification, we generated dual-reporter mice (PRURD2) by crossing D2.B10-Dmdmdx/J (D2-mdx) mice with FAP and brown/beige adipose tissue (BAT) reporter lines. Corresponding control mice (PRURDBA) were established on the DBA/2J background. At 12 months, heart, diaphragm, and tibialis anterior (TA) muscles were collected for histological analysis. FAPs were isolated via FACS and subjected to single-cell RNA sequencing. PRURD2 mice exhibited increased fibrosis across all muscles compared to controls (p < 0.01) and a significant rise in PDGFRα-GFP + FAPs (p < 0.05). UMAP clustering identified 11 distinct FAP subpopulations, with the fibrosis-associated CD55 cluster enriched in PRURD2 mice. Pseudotime analysis showed lineage progression from progenitor clusters toward the fibrogenic CD55 cluster. CellChat analysis indicated increased interactions in PRURD2 mice involving fibrosis-related pathways like COLLAGEN, TGF-β, WNT, NOTCH, and ANGPTL. Additionally, fibrosis-related signaling pathways such as THY1, TWEAK, EPHA, EPHB, and SEMA6 showed increased interactions among FAP clusters in PRURD2 mice. Differential gene expression analysis revealed top upregulated genes including Cxcl13, Cxcl3, Ly6d, Klk1, Fgf23, Serpinb2, Mmp13, Ccl17, Postn, and Adam12. PRURD2 mice develop severe fibrosis in skeletal and cardiac muscle, driven by FAP-induced signaling pathways and genes. This model is valuable for understanding muscle fibrosis in DMD and developing anti-fibrotic therapies.