Osteoclast
The cell that breaks bone down, releasing its mineral: the other half of remodelling.
Osteoclasts are the cells that break bone down. They attach to a bone surface, seal off a small area, and secrete acid and enzymes into it, dissolving the mineral and digesting the collagen underneath.
That sounds destructive and is essential. Bone is continuously remodelled, with osteoclasts removing old or damaged tissue and osteoblasts laying down new, and the whole skeleton is gradually replaced over years. Remodelling is how microdamage gets repaired and how bone reshapes itself in response to load.
Balance is what determines density. When formation matches resorption, density holds. When osteoclasts outpace osteoblasts, bone is lost, which is what happens in osteoporosis and, sharply, in women around the menopause as oestrogen falls, because oestrogen restrains osteoclast activity.
They are also the target of the main osteoporosis drugs. Bisphosphonates and denosumab work by suppressing osteoclast activity, slowing the removal side so formation can keep pace, which is a different strategy from stimulating new bone.
Mechanical loading influences them too, and this is where training enters. Strain from heavy or high impact loading shifts the remodelling balance towards formation, which is why the LIFTMOR trial's supervised twice weekly heavy resistance and impact training improved bone density in postmenopausal women with low bone mass.
Immobilisation does the reverse and does it fast. Bed rest and limb casting produce measurable bone loss within weeks, which is the same mechanism running in the other direction.
In practice, the actionable version is on our bone density entry: load bone heavily and progressively, keep calcium, vitamin D and protein adequate, and treat balance training as the other half of fracture prevention.