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Several risk factors of OA (e.g. genetics, age, and mechanical loading) have been identified1; however, the mechanisms of OA initiation and progression are yet to be understood.
Techniques using inert gas measuring permeability and connected porosity simultaneously under mechanical loading have been presented.
Experiments reveal that unit-cell shape, direction, type and magnitude of mechanical loading have significant effects on metamaterial anisotropic response and its instability characteristics.
The generation, equilibrium, and emission of dislocations from an elastically mismatched particle matrix interface under the combined effects of thermal and mechanical loading have been studied.
Several approaches to combine bone substitutes with biomolecules, cells or mechanical loading have been explored as an alternative to the limitation and risk-related bone auto- and allo-grafts.
The strain energy release rate components GI, GII and GIII along the annular shaped delamination front due to thermal residual stresses developed while curing the laminate (i.e., cooling from an elevated temperature of thermosetting to the room temperature) and the subsequent mechanical loading have been obtained by superimposing their respective effects.
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Passive mechanical loading has a beneficial effect on skeletal muscle function in sedated and mechanically ventilated ICU patients.
However, the role of sclerostin in age-related reduced adaptive (re)modeling (modeling and remodeling) to mechanical loading has never been investigated.
Dynamic mechanical loading has been reported to affect chondrocyte biosynthesis in both cartilage explant and chondrocyte-seeded constructs.
Furthermore, the application of mechanical loading has long been known to be a key player in the regulation of bone architecture and mechanical properties.
What is more, PTH and mechanical loading has a synergistic effect on bone formation, which is in favor of bone healing under physiological loading.
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