Question

Independentcy of osteoblast and osteoclastin bone remodelling is called as

Answer 1

In the bone-remodeling unit, the rate of osteoclast generation determines the extension of the bone-remodeling unit, whereas the life span of osteoclasts determines the depth of resorption. Although both genesis and apoptosis of osteoclasts lead to changes in osteoclast number and bone resorption, alteration of osteoclast life span might represent a more effective mechanism to accomplish rapid changes in bone resorption rate.

Sex steroids have profound effects on osteoclasts. Both estrogens and androgens inhibit osteoclast generation by regulating the production of pro-osteoclastogenic cytokines (such as IL-6 and IL-1) by cells of the stromal/osteoblastic lineage. Estrogens also induce apoptosis of mature osteoclasts. This, together with an inhibitory effect of the hormones on osteoblast generation, leads to attenuation of the rate of bone remodeling.

Mice receiving excess glucocorticoids exhibit reduced osteoclast progenitors, but cancellous osteoclast number does not decrease in the early phases of the disease, because glucocorticoids prolong the life span of preexisting osteoclasts. This effect may account for the early transient increase in bone resorption in patients with hyperglucocorticoidism. In contrast to the rapid prosurvival effect of glucocorticoids on mature osteoclasts, glucocorticoids induce a decrease in osteoclast formation caused by a reduction in the pool of osteoblastic cells that support osteoclastogenesis. This effect leads to the typical low remodeling rate observed in chronic glucocorticoid-induced osteoporosis.


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