Bone remodelling and the pathophysiology of osteoporosis
The remodelling cycle and the RANKL, OPG and Wnt-sclerostin signals that control it, why oestrogen loss, glucocorticoids and ageing cause bone loss, how T-scores and turnover markers are read, and how each osteoporosis drug targets the cycle.
Tier 1Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- Bone is renewed constantly by basic multicellular units: osteoclasts resorb, osteoblasts refill. About 10% of the adult skeleton is replaced each year, trabecular bone faster than cortical.
- Osteocytes are the controllers. They sense load and make RANKL (drives resorption), sclerostin (blocks formation) and FGF23.
- Osteoporosis develops when resorption exceeds formation in each cycle (negative remodelling balance) and turnover is high, so more cycles each lose bone. Peak bone mass at about age 30 sets the starting point.
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Sources
- Williams Textbook of Endocrinology, 15th editionElsevier, 2024
- Osteoporosis management and fracture prevention in postmenopausal women and men over 50 years of age, 3rd editionAU/NZRACGP and Healthy Bones Australia, 2024
- 2024 RACGP and Healthy Bones Australia guideline for osteoporosis management and fracture prevention (summary)AU/NZMedical Journal of Australia, 2025
- Denosumab for prevention of fractures in postmenopausal women with osteoporosis (FREEDOM)New England Journal of Medicine, 2009
- Romosozumab or alendronate for fracture prevention in women with osteoporosis (ARCH)New England Journal of Medicine, 2017
- New treatment announced on PBS (abaloparatide)AU/NZHealthy Bones Australia, August 2026
- Last updated
- 14 November 2026
What changed
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