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It is known that excessive mechanical force exerted by hyperocclusion induces occlusal trauma.
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Contrarily, excessive mechanical forces can induce inflammation via activation of the NF-κB signaling cascade.Given the osteogenic potential of mechanical signals, it is imperative to exploit their therapeutic efficacy for the treatment of bone disorders.
Since OA is often a consequence of excessive mechanical forces [1] and given that the application of high fluid shear to chondrocytes recapitulates some of the earmarks of OA [4], [6], [7], [8], [9], we aimed to screen the gene expression profiles of shear-activated chondrocytes and assess potential similarities with OA chondrocytes.
However, excessive mechanical action leads to interface damage.
The source of this extrinsic mechanical force remains unknown.
Mechanical force significantly increased solid loss by causing surface erosion.
According to our experience, the adjustment of the pulse duration in this range may avoid the possibility of strong mechanical forces and excessive heating in the substrate, as it has been observed with standard Nd YAG laser systems.
This provides a strong scaffold that attaches to the epidermis to prevent the epidermis from undergoing excessive deformation while it experiences mechanical forces.
Excessive joint contact forces, in particular loading conditions under which the mechanical forces are transferred disproportionally across the tibiofemoral joint, are considered to be a driving factor of osteoarthritis (OA) (3).
Patients with excessive lateral torsion of the tibia may fail conservative management since it does not address the underlying mechanical forces at the knee caused by the torsion.
Mechanical forces are central to developmental, physiological and pathological processes1.
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