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Changes found in the graft architecture correspond to changes expected after functional adaptation to loading.
Adaptation to loading seems to occur in a site-specific fashion by gross geometric changes, structural or architectural changes, or by their combination.
Deciphering the mechanisms by which changes in the mechanical environment regulate sclerostin production may lead to the development of therapeutic strategies that can reverse the skeletal structural deterioration characteristic of disuse and age-related osteoporosis and enhance bones' functional adaptation to loading.
To successfully carry out this locomotive function, the bone tissue is equipped with a mechano-sensory system that facilitates the skeletal adaptation to loading.
This effect in humans also occurs in mice which experience age-related bone loss and reduced adaptation to loading.
The adaptation to loading can ultimately lead to increases in CSA and collagen content in chronically loaded tendons [ 5].
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An in vitro model was used to investigate the effect of mechanical stimuli on adaptation to load and calcium signaling in aligned medial collateral ligament cells (MCL).
The tendon becomes less efficient at adaptation to load.
During bone remodeling (reconstruction, lifetime adaptation to load and age), osteoclasts resorb a small volume of bone at a distinct location at the inner site of the cortex adjacent to the marrow [ 10].
Experiments to investigate bone's physiological adaptation to mechanical loading frequently employ models that apply dynamic loads to bones in vivo and assess the changes in mass and architecture that result.
ERs can also be stimulated by mechanical loading (Galea et al., 2013), with bone adaptation to mechanical loading requiring ERα (Lee et al., 2003).
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