Osteomalacia
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Direct answer
Diffuse bone pain, proximal muscle weakness and a waddling gait in an adult with low or low-normal calcium, low phosphate, raised alkaline phosphatase, low vitamin D and secondary hyperparathyroidism — this is osteomalacia, defective mineralisation of osteoid in the adult (the same defect before growth-plate fusion is rickets), most often from vitamin D deficiency. Looser's zones (pseudofractures) on radiographs are the classic finding, and treatment is cholecalciferol replacement with calcium.
What you must remember
- Mineralisation failure: vitamin D deficiency (dark skin, veiling, poor sun exposure, malabsorption, chronic kidney disease), hypophosphataemia (X-linked hypophosphataemic rickets, renal phosphate wasting, tumour-induced osteomalacia from phosphaturic mesenchymal tumours) and enzyme-inducing antiepileptics (phenytoin, carbamazepine, phenobarbitone) that accelerate vitamin D catabolism.
- Biochemistry: low calcium, low phosphate, high alkaline phosphatase (bone origin), low 25-hydroxyvitamin D, elevated PTH; in pure hypophosphataemic forms calcium and PTH are near normal while phosphate is strikingly low with renal phosphate wasting.
- Looser's zones — symmetrical, poorly healing cortical stress fractures along the scapulae, lateral femoral cortices, pubic rami and ribs — are radiologically characteristic; there may also be vertebral biconcavity, triradiate pelvis and pseudowidening of growth plates in children with rickets.
- Clinical: bone pain and tenderness, proximal myopathy (difficulty rising from sitting, waddling gait, Gower-positive pattern), deformity in longstanding disease and hypocalcaemic symptoms in severe deficiency.
- Treatment: cholecalciferol loading (for example 60,000 international units weekly for 6 to 8 weeks in Indian practice) then maintenance of 1,000 to 2,000 international units daily, with elemental calcium 1 to 1.2 g daily; monitor calcium, phosphate and alkaline phosphatase.
- Special situations: renal disease needs active vitamin D analogues (alfacalcidol, calcitriol); hypophosphataemic disease needs phosphate supplementation with calcitriol; tumour-induced osteomalacia is cured by removing the tumour.
- Myopathy plus fractures with a normal muscle biopsy should prompt vitamin D measurement rather than a primary muscle disease work-up.
A veiled woman who cannot rise from a chair
A 58-year-old woman who stays indoors and is veiled outdoors reports a year of generalized bone pain and difficulty rising from sitting, with a waddling gait — the proximal myopathy pattern that should prompt vitamin D measurement rather than a primary muscle disease work-up. The biochemistry quartet reads the diagnosis: calcium 8.1, phosphate 2.0, alkaline phosphatase markedly raised (bone origin), 25-hydroxyvitamin D 8 ng per mL, PTH elevated — secondary hyperparathyroidism driving phosphate wasting on top of deficient mineralisation. Ask why she is deficient: poor sun exposure, dark skin and veiling (the dominant Indian causes), malabsorption, chronic kidney disease; if calcium and PTH were near normal while phosphate was strikingly low with renal phosphate wasting, the lane shifts to hypophosphataemic forms — X-linked hypophosphataemic rickets, renal wasting, or tumour-induced osteomalacia from FGF-23-secreting phosphaturic mesenchymal tumours, cured by removing the tumour. Her radiographs show Looser's zones — symmetrical, poorly healing cortical stress fractures along the scapulae, lateral femoral cortices, pubic rami and ribs — with vertebral biconcavity in advanced disease; the child equivalent adds triradiate pelvis and widened physes. Treat with cholecalciferol loading, in Indian practice commonly 60,000 international units weekly for six to eight weeks, then 1,000 to 2,000 units daily, with elemental calcium 1 to 1.2 g, monitoring calcium, phosphate and alkaline phosphatase; If she were on phenytoin, carbamazepine or phenobarbitone, remember that enzyme induction accelerates vitamin D catabolism — antiepileptic osteomalacia is a stem in itself.
Where students slip
The osteoporosis contrast is among the most repeated comparisons in the paper and still catches candidates: both fracture, but osteoporosis is reduced quantity of normally mineralised bone with normal biochemistry, while osteomalacia is normal quantity of poorly mineralised osteoid with the abnormal quartet and Looser's zones. The radiology nuance follows — Looser's zones mimic fracture lines but are symmetrically placed and not truly traumatic. Rickets versus osteomalacia is purely the age distinction of physeal closure. And the alkaline phosphatase raised "for liver work-up" is the quiet trap: when bone-origin enzyme and bone pain coexist, fractionate it and measure vitamin D.
Frequently asked questions
What is the difference between rickets and osteomalacia?
The same mineralisation defect before growth-plate fusion is rickets (with skeletal deformity and widened physes); after fusion it is osteomalacia.
What are Looser's zones?
Pseudofractures — symmetric cortical radiolucent stress fractures of the scapulae, lateral femoral shafts, pubic rami and ribs characteristic of osteomalacia.
What biochemistry defines vitamin D osteomalacia?
Low calcium, low phosphate, raised alkaline phosphatase, deficient 25-hydroxyvitamin D and secondary elevation of PTH.
Which drugs cause osteomalacia?
Enzyme-inducing antiepileptics (phenytoin, carbamazepine, phenobarbitone), chronic aluminium exposure and long-term excessive antacid or phosphate-binding use.
What is tumour-induced osteomalacia?
Phosphate-wasting osteomalacia caused by phosphaturic mesenchymal tumours secreting FGF-23; surgical removal of the tumour cures it.
How is osteomalacia treated?
Cholecalciferol loading followed by maintenance, plus calcium; active vitamin D analogues and phosphate are needed in renal disease and hypophosphataemic forms.