Tissue‐engineered menisci hold promise as an alternative to allograft procedures but require a means of robust fixation to the native bone. The insertion of the meniscus into bone is critical for meniscal function and inclusion of a soft tissue‐to‐bone interface in a tissue engineered implant can aid in the fixation process. The native insertion is characterized by gradients in composition, tissue architecture, and cellular phenotype, which are all difficult to replicate. In this study, a soft tissue‐to‐bone interface is tissue engineered with a cellular gradient of fibrochondrocytes and mesenchymal stem cells and subjected to a biochemical gradient through a custom media diffusion bioreactor. These constructs, consisting of interpenetrating collagen and boney regions, display improved mechanical performance and collagen organization compared to controls without a cellular or chemical gradient. Media gradient exposure produces morphological features in the constructs that appear similar to the native tissue. Collectively, these data show that cellular and biochemical gradients improve integration between collagen and bone in a tissue engineered soft tissue‐to‐bone construct.

Objective Obesity and osteoarthritis (OA) are 2 major public health issues affecting millions of people worldwide. Whereas parental obesity affects the predisposition to diseases such as cancer or diabetes in children, transgenerational influences on musculoskeletal conditions such as OA are poorly understood. This study was undertaken to assess the intergenerational effects of a parental/grandparental high‐fat diet on the metabolic and skeletal phenotype, systemic inflammation, and predisposition to OA in 2 generations of offspring in mice. Methods Metabolic phenotype and predisposition to OA were investigated in the first and second (F1 and F2) generations of offspring (n = 10–16 mice per sex per diet) bred from mice fed a high‐fat diet (HFD) or a low‐fat control diet. OA was induced by destabilizing the medial meniscus. OA, synovitis, and adipose tissue inflammation were determined histologically, while bone changes were measured using micro–computed tomography. Serum and synovial cytokines were measured by multiplex assay. Results Parental high‐fat feeding showed an intergenerational effect, with inheritance of increased weight gain (up to 19% in the F1 generation and 9% in F2), metabolic imbalance, and injury‐induced OA in at least 2 generations of mice, despite the fact that the offspring were fed the low‐fat diet. Strikingly, both F1 and F2 female mice showed an increased predisposition to injury‐induced OA (48% higher predisposition in F1 and 19% in F2 female mice fed the HFD) and developed bone microarchitectural changes that were attributable to parental and grandparental high‐fat feeding. Conclusion The results of this study reveal a detrimental effect of parental HFD and obesity on the musculoskeletal integrity of 2 generations of offspring, indicating the importance of further investigation of these effects. An improved understanding of the mechanisms involved in the transmissibility of diet‐induced changes through multiple generations may help in the development of future therapies that would target the effects of obesity on OA and related conditions.

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While it is well known that mechanical signals can either promote or disrupt intervertebral disc (IVD) homeostasis, the molecular mechanisms for transducing mechanical stimuli are not fully understood. The transient receptor potential vanilloid 4 (TRPV4) ion channel activated in isolated IVD cells initiates extra-

Collagen is a major structural component of nearly every tissue in the human body, whose hierarchical organization imparts specific mechanical properties and defines overall tissue function. Collagenous soft tissues are dynamic structures that are in a constant state of remodeling but are also prone to damage and pathology. Optical techniques are uniquely suited for imaging collagen in these dynamic situations as they allow for non-invasive monitoring with relatively high spatiotemporal resolution. This review presents an overview of common collagen dynamic processes associated with human health and disease and optical imaging approaches that are uniquely suited for monitoring, sensing, and diagnosing these changes. This review aims to 1) provide researchers with an understanding of the underlying optical properties of collagen that can be leveraged for extracellular matrix visualization and 2) present emerging opportunities for machine learning approaches to drive multiscale and multimodality solutions.

Recent advancements in nanofabrication technology has led to commercialization of single-chip polarization and color-polarization imaging sensors in the visible spectrum. Novel applications have arisen with the emergence of these sensors leading to questions about noise in the reconstructed polarization images. In this paper, we provide theoretical analysis for the input and output referred noise for the angle and degree of linear polarization information. We validated our theoretical model with experimental data collected from a division of focal plane polarization sensor. Our data indicates that the noise in the angle of polarization images depends on both incident light intensity and degree of linear polarization and is independent of the incident angle of polarization. However, noise in degree of linear polarization images depends on all three parameters: incident light intensity, angle and degree of linear polarization. This theoretical model can help guide the development of imaging setups to record optimal polarization information.

Mechanical factors such as stress in the extracellular environment are known to affect phenotypic commitment of cells. However, the stress fields experienced by cells in tissues are multiaxial, and the ways that cells integrate this multiaxial information are largely unknown. Here, we report that the anisotropy of these stress fields is a critical factor triggering phenotypic transition in fibroblast cells, outweighing the previously reported role of stress amplitude. Using a combined experimental and computational approach, we discovered a self-reinforcing mechanism in which cellular protrusions interact with collagen fibers to develop tension anisotropy, which in turn stabilizes protrusions and amplifies their contractile forces. Disruption of this self-reinforcing process, either by reducing tension anisotropy or by inhibiting contractile protrusions, prevented phenotypic conversion of fibroblasts to contractile myofibroblasts.

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