Evidence brief
Bone Remodeling and Osteoporosis
Bone remodeling: coupled osteoclast-osteoblast activity
RANK-RANKL-OPG pathway central to regulation
Estrogen deficiency increases bone resorption
Type I (postmenopausal) and Type II (senile) osteoporosis
Trabecular bone lost before cortical
Understanding osteoporosis pathophysiology guides pharmacological treatment targets and explains patterns of fragility fracture.
Know RANK-RANKL-OPG: RANKL activates osteoclasts via RANK receptor; OPG is decoy receptor. Estrogen reduces RANKL, increases OPG. Bisphosphonates inhibit osteoclasts. Denosumab is anti-RANKL. Teriparatide (PTH) stimulates osteoblasts. Clinical implications for fracture fixation in osteoporotic bone.
Riggs BL, Khosla S, Melton LJ. A unitary model for involutional osteoporosis: estrogen deficiency causes both type I and type II osteoporosis in postmenopausal women and contributes to bone loss in aging men. J Bone Miner Res. 1998;13(5):763-773.
Level III
Retrospective comparative study or case-control study