PassFinals
Musculoskeletal

Osteomalacia

Osteomalacia is defective mineralisation of newly formed adult bone, most often from vitamin D deficiency or phosphate depletion. It causes diffuse bone pain, proximal weakness and fragility or pseudofractures, with a pattern of abnormal mineral metabolism rather than the normal biochemistry of osteoporosis.

In a nutshell

Osteomalacia is defective mineralisation of adult bone, usually from vitamin-D deficiency but also from calcium or phosphate depletion, renal or liver disease, malabsorption or medicines. Think of diffuse bone pain, proximal weakness and fragility or pseudofractures. Check mineral metabolism and 25-hydroxyvitamin D when clinically indicated, treat the cause and replace vitamin D or calcium safely through current BNF or specialist pathways.

Classic presentation

An adult with diffuse pelvic or rib pain, proximal weakness and difficulty rising from a chair has a raised alkaline phosphatase with disordered calcium, phosphate and parathyroid hormone. Check vitamin D and the cause, while considering fracture and malignancy.

Key points

  • Osteomalacia is a mineralisation defect; rickets is the analogous disorder at open growth plates.
  • The common pattern is raised alkaline phosphatase with low or low-normal phosphate, normal or low calcium and raised parathyroid hormone, but patterns vary by cause.
  • Bone pain plus proximal weakness and impaired mobility is more suggestive of osteomalacia than osteoporosis, which usually has normal routine biochemistry.
  • Looser zones are pseudofractures and support the diagnosis in the right biochemical context.
  • Measure 25-hydroxyvitamin D when symptoms or bone disease make the result clinically useful, not as indiscriminate screening.
  • Replace vitamin D and calcium using current BNF or local NHS pathways, and investigate malabsorption, renal, liver, medication and phosphate-wasting causes.
  • Persistent hypophosphataemia, renal impairment, hypercalcaemia, recurrent fractures or failure to improve requires specialist review.

First-line investigation

Bone profile, phosphate, parathyroid hormone, renal and liver function, with 25-hydroxyvitamin D when osteomalacia or clinically important vitamin-D deficiency is suspected.

Management

Identify hypocalcaemia and fracture emergencies

  • Escalate tetany, seizures, arrhythmia, severe weakness or suspected major fragility fracture; check calcium and renal function before high-dose replacement.3,2

Confirm the mineralisation problem and cause

  • Check calcium, phosphate, alkaline phosphatase, parathyroid hormone, renal and liver function, then measure 25-hydroxyvitamin D when clinically indicated.1,2,3
  • Investigate malabsorption, renal or liver disease, medicines and phosphate wasting when the pattern is atypical or treatment does not work.1,3

Replace deficient minerals safely

  • Use current BNF or local NHS pathways for vitamin-D replacement, maintenance and calcium supplementation; do not substitute a remembered prevention dose.3,1,5

Treat the underlying disease and protect bone

  • Treat coeliac or other malabsorption, review medicines and refer renal, hepatic or phosphate-wasting disease; manage fractures, falls and mobility while bone recovers.1,3,2

Confirm clinical and biochemical recovery

  • Review pain, strength, mobility, fractures, calcium, phosphate, alkaline phosphatase, parathyroid hormone and renal function when clinically indicated, and refer if response is incomplete or atypical.1,3

Exam traps

  • A normal serum calcium does not exclude vitamin-D-deficiency osteomalacia because secondary hyperparathyroidism can maintain it.
  • A low vitamin-D result alone does not prove that diffuse pain is osteomalacia; correlate it with symptoms, examination and mineral biochemistry.
  • Osteoporosis is usually painless until fracture and has normal routine bone biochemistry; do not use low bone density alone to diagnose osteomalacia.
  • Chronic kidney disease, renal phosphate wasting and malabsorption may need specialist treatment rather than ordinary colecalciferol alone.
  • Do not use a prevention dose as a treatment regimen for established osteomalacia, and do not quote a paediatric or adult loading regimen from memory.
  • Persistent pain, abnormal phosphate or no biochemical response should prompt review of adherence, diagnosis and underlying cause.

Illustrations

Severe osteomalacia on radiographsRadiographic example of severe osteomalacia with diffuse osteopenia and pathological or pseudofracture changes. The image should be checked for diagnostic legibility and teaching value in the separate image campaign.Leslie Gamache and Mark R. Burge, Wikimedia Commons · CC-BY-3.0

Key sources

  1. NICE CKS, Vitamin D deficiency in adults (Current NICE Clinical Knowledge Summary for adult vitamin-D deficiency testing and treatment; direct access was restricted in this environment, so unsupported numeric regimens are omitted)
  2. NHS, Rickets and osteomalacia (NHS condition information, last reviewed 9 July 2025)Updated 9 Jul 2025
  3. BNF, colecalciferol and calcium preparations (Current UK prescribing source for treatment choice, contraindications, interactions, monitoring and dosing; detailed regimen claims are omitted because BNF access was restricted and no browser session was available)
  4. NHS, Vitamin D (NHS prevention information and safety limits; last reviewed 3 August 2020)Updated 3 Aug 2020
  5. NHS, How and when to take colecalciferol (NHS medicine information for maintenance and loading treatment; use BNF and local policy for individual prescribing)

This page is exam revision material, not medical advice, and must not be used for patient care. Always check drug doses against the BNF and current guidance. Full disclaimer.