osteoclast
If osteoblasts are the builders, osteoclasts are the demolition crew. These large, many-nucleus cells clamp onto bone and dissolve it, breaking down old or damaged tissue and releasing its stored calcium back into the blood.
An osteoclast works by sealing a patch of bone, then pumping acid and digestive enzymes into the sealed space to dissolve both the mineral and the collagen beneath it. They are not made from the same lineage as osteoblasts; they descend from blood-cell precursors. Their formation depends on the signal RANKL, supplied by osteoblasts and other cells, so osteoclasts are ultimately controlled by the very cells they work alongside. PTH boosts their activity indirectly through this RANKL pathway.
Overactive osteoclasts drive bone loss in osteoporosis, in hyperparathyroidism, and in cancers that spread to bone. This makes them a prime drug target: bisphosphonates poison their function, and denosumab blocks RANKL to stop them forming at all. Suppressing osteoclasts too completely, however, can cause rare problems because some resorption is needed for healthy bone repair.
Denosumab treats osteoporosis by blocking RANKL, the signal osteoclasts need to form, so far fewer of them appear and bone breakdown drops sharply.
Blocking RANKL starves osteoclasts of the signal they need.
Osteoclasts come from the same family as macrophages (immune scavenger cells), not from bone-building cells, which is why immune-related signals influence bone so strongly.