Shape memory alloy actuated ankle foot orthosis for reduction of locomotion force

peer reviewedHumans can be considered inefficient at walking because they are unable to achieve the theoretically ideal 'zero energy cost' of steady-state locomotion that is possible for bipeds who have elastic tissues. This inefficiency is mainly due to part of the energy that is generated by the body to complete a single step being dissipated instead of being stored for use in the proceeding step. This suggests that we can improve locomotion efficiency and reduce the metabolic energy cost of walking by manipulating the elasticity of the lower limbs using exoskeletal devices [1]. However, most traditional designs use springs made from regular material that have a constant stiffness. These devices exert a linear force pattern that is not biocompatible because they do not mimic the forces of the muscles or the tendons of the human body. This paper presents an interdisciplinary study of the design of a passive-dynamic ankle foot orthosis mechanism that reduces the biological muscle force requirements during locomotion, thus reducing the metabolic energy cost of walking while maintaining biocompatibility. Shape memory alloy is used as a smart material for an actuator owing to its super-elasticity. This super-elasticity provides a nonlinear stiffness pattern that generates forces comparable to those of healthy muscles

Cartilaginous endplates: A comprehensive review on a neglected structure in intervertebral disc research

The cartilaginous endplates (CEP) are key components of the intervertebral disc (IVD) necessary for sustaining the nutrition of the disc while distributing mechanical loads and preventing the disc from bulging into the adjacent vertebral body. The size, shape, and composition of the CEP are essential in maintaining its function, and degeneration of the CEP is considered a contributor to early IVD degeneration. In addition, the CEP is implicated in Modic changes, which are often associated with low back pain. This review aims to tackle the current knowledge of the CEP regarding its structure, composition, permeability, and mechanical role in a healthy disc, how they change with degeneration, and how they connect to IVD degeneration and low back pain. Additionally, the authors suggest a standardized naming convention regarding the CEP and bony endplate and suggest avoiding the term vertebral endplate. Currently, there is limited data on the CEP itself as reported data is often a combination of CEP and bony endplate, or the CEP is considered as articular cartilage. However, it is clear the CEP is a unique tissue type that differs from articular cartilage, bony endplate, and other IVD tissues. Thus, future research should investigate the CEP separately to fully understand its role in healthy and degenerated IVDs. Further, most IVD regeneration therapies in development failed to address, or even considered the CEP, despite its key role in nutrition and mechanical stability within the IVD. Thus, the CEP should be considered and potentially targeted for future sustainable treatments

Immuno-modulatory effects of intervertebral disc cells

Low back pain is a highly prevalent, chronic, and costly medical condition predominantly triggered by intervertebral disc degeneration (IDD). IDD is often caused by structural and biochemical changes in intervertebral discs (IVD) that prompt a pathologic shift from an anabolic to catabolic state, affecting extracellular matrix (ECM) production, enzyme generation, cytokine and chemokine production, neurotrophic and angiogenic factor production. The IVD is an immune-privileged organ. However, during degeneration immune cells and inflammatory factors can infiltrate through defects in the cartilage endplate and annulus fibrosus fissures, further accelerating the catabolic environment. Remarkably, though, catabolic ECM disruption also occurs in the absence of immune cell infiltration, largely due to native disc cell production of catabolic enzymes and cytokines. An unbalanced metabolism could be induced by many different factors, including a harsh microenvironment, biomechanical cues, genetics, and infection. The complex, multifactorial nature of IDD brings the challenge of identifying key factors which initiate the degenerative cascade, eventually leading to back pain. These factors are often investigated through methods including animal models, 3D cell culture, bioreactors, and computational models. However, the crosstalk between the IVD, immune system, and shifted metabolism is frequently misconstrued, often with the assumption that the presence of cytokines and chemokines is synonymous to inflammation or an immune response, which is not true for the intact disc. Therefore, this review will tackle immunomodulatory and IVD cell roles in IDD, clarifying the differences between cellular involvements and implications for therapeutic development and assessing models used to explore inflammatory or catabolic IVD environments