Metabolic Bone Disease and Osteoporosis
Osteoporosis essentials
Osteoporosis is reduced bone strength leading to fragility fracture. Diagnose by dual-energy X-ray absorptiometry T-score of −2.5 or below, or by a fragility fracture of hip or spine regardless of T-score. FRAX estimates 10-year fracture probability and helps decide treatment in osteopenia. Secondary causes must be excluded: glucocorticoid use, hyperthyroidism, hyperparathyroidism, vitamin D deficiency, malabsorption, hypogonadism, myeloma and malignancy.
Management logic
Address calcium and vitamin D intake, weight-bearing and balance exercise, smoking and alcohol, and falls risk. Bisphosphonates are first line for most; check renal function and dental status before intravenous therapy. Denosumab requires adherence and must not be stopped abruptly without transition planning because of rebound vertebral fracture risk. Teriparatide is anabolic and used for severe disease. Always consider drug holidays for bisphosphonates after long-term use.
Other metabolic bone disease
- Osteomalacia: defective mineralisation, bone pain, proximal myopathy, low phosphate/calcium, raised alkaline phosphatase; causes include vitamin D deficiency and renal phosphate wasting.
- Paget disease: raised alkaline phosphatase with normal calcium, bone pain and deformity; risk of osteosarcoma and deafness.
- Primary hyperparathyroidism: hypercalcaemia with raised PTH, "stones, bones, abdominal groans, psychic moans".
- Osteonecrosis: risk with glucocorticoids, alcohol, sickle cell disease; imaging is often needed before radiographs change.
Traps
- A normal T-score does not exclude fragility fracture risk.
- Alkaline phosphatase is raised in Paget disease but calcium is normal.
- Glucocorticoid-induced osteoporosis occurs early and rapidly; assess bone health at steroid initiation.
Rule of thumb
Fragility fracture equals osteoporosis until proven otherwise - investigate secondary causes and start bone protection.