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It has been suggested that suppression of proliferation and maturation of OCs prevents excess bone loss.
The presence of tumor cells in the bone microenvironment perturbs the balance between osteoblasts and osteoclasts, leading to excess bone loss or formation.
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Close monitoring for excessive bone loss and anemia is important.
We observed that excess Dex resulted in bone loss and increased marrow fat in our model.
Population studies indicate that hormone deficiency and hormone excess are associated with increased bone loss and fracture risk [ 68].
Thus, low Ca intakes may increase CVD risks and bone loss, whereas excess Ca intakes may lead to Ca deposition in the arteries or vascular calcification, and could therefore increase the risks of CVD [ 11].
Unlike the chronic parathyroid hormone excess of hyperparathyroidism, which leads to bone loss, teriparatide is given as a once daily subcutaneous bolus injection.
In RA, focal bone loss is due to excess bone resorption by osteoclasts.
Phosphate plays essential biological roles and its plasma level in humans requires tight control to avoid bone loss (insufficiency) or vascular calcification (excess).
In osteoblasts, mesenchymal cells that are developmentally closely related to synovial fibroblasts, glucocorticoids are a very powerful inducer of DKK1 and this effect has been proposed as the mechanism that mediates bone loss due to systemic glucocorticoid excess [ 14].
In addition, "simple" interventions aiming at the management of body weight in older adults are controversial, because any weight loss, whether intentional or not, may have harmful effects by promoting sarcopenia, bone loss, nutritional deficiencies, and even excess mortality in older adults.
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