Objective: Women have a higher prevalence and burden of joint injuries and pathologies involving articular cartilage than men. Although knee injuries affecting young women are on the rise, most studies related to sexual dimorphism target postmenopausal women. We hypothesize that sexual dimorphism in cartilage structure and mechanics is present before menopause, which can contribute to sex disparities in cartilage pathologies. Design: Bovine knee was used as a model to study healthy adult cartilage. We compared elastic moduli under compression, abundances of extracellular and pericellular matrix (PCM) proteins using proteomics, and PCM constituency with tissue immunofluorescence. The gene expression of matrix-related genes under basal, anabolic, and catabolic conditions was assessed by quantitative polymerase chain reaction (qPCR). Results: The equilibrium modulus was higher in male cartilage compared with female cartilage. Proteoglycans were not associated with this biomechanical dimorphism. Proteomic and pathway analyses of tissue showed dimorphic enriched pathways in extracellular matrix (ECM)-related proteins in which male cartilage was enriched in matrix interconnectors and crosslinkers that strengthen the ECM network. Moreover, male and female tissue differed in enriched PCM components. Females had more abundance of collagen type VI and decorin, suggesting different PCM mechanics. Furthermore, the activation of regenerative and catabolic function in chondrocytes triggered sex-dependent signatures in gene expression, indicating dimorphic genetic regulation that is dependent on stimulation. Conclusions: We provide evidence for sexual dimorphism in cartilage before menopause. Some differences are intrinsic to chondrocytes’ gene expression defined by their XX versus XY chromosomal constituency.

Intravascular stents for pediatric patients that degrade without inhibiting vessel growth remain a clinical challenge. Here, poly(L-lactide) fibers (DH-BDS) at two thicknesses, 250 μm and 300 μm, were assembled into large, pediatric-sized stents (Ø10 - Ø20 mm). Fibers were characterized mechanically and thermally, then stent mechanical properties were compared to metal controls, while mass loss and degradation kinetics modeling estimated total stent degradation time. Thicker fibers displayed lower stiffness (1969 ± 44 vs 2126 ± 37 MPa) and yield stress (117 ± 12 vs 137 ± 5 MPa) than thinner counterparts, but exhibited similar fail strength (478 ± 28 vs 476 ± 16 MPa) at higher strains (47 ± 2 vs 44 ± 2%). Stents all exhibited crystallinity between 51.3 - 54.4% and fiber glass transition temperatures of 88.6 ± 0.5 °C and 84.6 ± 0.5 °C were well above physiological ranges. Radial strength (0.31 ± 0.01 - 0.34 ± 0.02 N/mm) in thinner stents was similar to metal stents (0.24 - 0.41 N/mm) up to Ø14 mm with no foreshortening and thicker coils granted comparable radial strength (0.32 ± 0.02 - 0.34 ± 0.02 N/mm) in stents larger than Ø14 mm. Both 10 mm (1.17 ± 0.02 % and 0.86 ± 0.1 %) and 12 mm (1.1 ± 0.03% and 0.89 ± 0.1%) stents exhibited minimal weight loss over one year. Degradation kinetics models predicted full stent degradation within 2.8 - 4.5 years depending on thickness. DH-BDS exhibiting hoop strength similar to metal stents and demonstrating minimal degradation and strength loss over the first year before completely disappearing within 3 to 4.5 years show promise as a pediatric interventional alternative to current strategies.