As the estrogen is combined with osteoclast, it can inhibit the activity of lysomal enzyme, inhibit bone resorption and decrease the ability of osteclast on forming cavate in bone slice.
It does this by stimulating osteoclasts, the cells that break bone down, to release hydrogen ions which dissolves the hard, mineralized hydroxyapatite.
They're like the construction foremen of your bones, passing along commands to your skeleton's two main workhorses: the osteoblasts and the osteoclasts.
When the old bone tissue is cleaned out, the osteoclasts then undergo apoptosis, where they basically self-destruct before they can do any more damage.
Because your immune system rushes to the rescue, sending in special cells called osteoclasts, which ultimately relieve the pressure and restore blood flow.
With senile osteoporosis, on the other hand, it's believed that osteoblasts just gradually lose the ability to form bone, while the osteoclasts keep doing their thing unabated.
Finally, medications like denosumab, which is a monoclonal antibody that inhibits osteoclasts, and raloxifene, which is a selective estrogen receptor modulator, can be used for postmenopausal osteoporosis.
So while your osteoblasts are the bone-makers, your osteoclasts are the bone-breakers — which is a kind of violent image. Maybe think of them as like a bone-breaker-downer.
But, for reasons that we don't understand yet, the osteoclasts actually increase their rate of bone resorption in low gravity, while the osteoblasts dial back on the bone formation.
The tumor cells arises from osteoclasts cells, but then develop into cells that have numerous nuclei - typically over 50 nuclei - so you can think of them as destructive little giants.