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Bone resorption can be inhibited by several strategies.
Stimulation of PTH synthesis and bone resorption can be caused as the result of low levels of vitamin D. Continuance insufficiency of vitamin D results in rickets and osteomalacia, with skeletal deformities in children and bone pain and increased risk of fractures in adults [33].
Although the enhanced bone resorption can be inhibited by a treatment with bisphosphonates [4], [5], it has been difficult to stimulate the unloading-induced suppression of bone formation.
Bone resorption can be reduced by bisphosphonates.
The progress of callus formation and bone resorption can be seen at 6 and 9 weeks.
The presented data suggest that bone resorption can be strongly attenuated without the secondary positive effects on cartilage degradation.
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The net amount of bone formation and resorption can be crudely assessed by bone turnover markers that are routinely measured in many laboratories.
Since bone formation and resorption can be uncoupled and are independent processes, the upregulation of OPG alone might tip the balance towards bone formation [49].
Collagen breakdown, and thus bone resorption, can now be assessed by measuring the urinary excretion of the collagen crosslinks, pyridinoline (Pyd) and deoxypyridinoline (Dpd).
The protective effect of DAP12 on ovariectomy-induced bone loss has been emphasized since we show here that bone resorption activity can be restored after ovariectomy of Dap12 loss of function mutant mice.
Increased bone resorption due to increased osteoclast formation has been proposed, and the pharmacological inhibition of bone resorption can prevent bone loss in animal models.
More suggestions(16)
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