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Osteomalacia and Rickets

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Original article by Tom Leach | Last updated on 27/5/2014

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In This Article
Introduction
Causes
Clinical Features
In children
Investigations
Treatment

Introduction
These are essentially the same disorder. In children, the disease is rickets but after fusion of the
epiphyseal plates it is known as osteomalacia.
The most common cause is vitamin D deficiency.
The condition is characterised by normal bone formation with abnormal bone mineralisation,
thus there is excess osteoid and cartilage, and insufficient bone.

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Causes
Vitamin D deficiency due to lack of sunlight insufficient dietary intake. Both often occur
simultaneously. Common in the elderly (e.g. often indoors for long periods) and also in

dark skinned populations residing in non-native climes (e.g. in the UK) particularly if
they cover up their skin (e.g. common in Inidan Pakistani women and girls in the UK. As a
result, chapatti flour is fortified with vitamin D).
Renal osteomalacia resulting in vitamin D deficiency. Often occurs in patients with longterm renal pathologies.
Drug Induced particularly with anticonvulsants
Vitamin D resistant rickets / osteomalacia a collection of inherited diseases, including
familial hypophosphataemia, and a disorder where the vitamin D receptor is defective.
Type I hereditary vitamin D-dependent rickets caused by ineffective conversion of
vitamin D precursors in the kidneys (25()H)D to 1,25(OH)D. Autosomal recessive
Type II hereditary vitamin D-dependent rickets due to mutations in the 1,25(OH)D
receptor, causes end-organ resistance to vitamin D
Both are treated with high levels of calcitriol ( 1,25()H)2vitamin D )
Hypoparathyroidism
Low dietary calcium / phosphate (rare)

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Clinical Features
Muscle aches
Muscle weakness
Bone Pain / pain on walking
Predisposition to fractures especially in the elderly
Tetany parasthesia of the lips, tongue and face, sometimes facial and carpopedal spasm,
rarely seizures. May be hard to distinguish from other causes of seizure.

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In children

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Generally unwell
Delayed walking / crawling / sitting
In pregnancy, amy affect the foetus, especially the skull of the newborn (pingpong ball
like skull - craniotabes)
Craniotabes is also seen in syphilis, and neonates with this are often tested for the
disease.
Rachitic Rosary bead like nodules on the ribs
Kyphoscoliosis
Bowed legs and knock knees only occur in severe cases in older children

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Investigations
Vit D often

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Alkaline phosphate: may be or

Parathyroid hormone
Calcium
Low vitamin D results in low absorption of calcium in the diet, which inturn stimulates
increased PTH production. High levels of PTH also increase phosphate excretion, but may
normalise serum calcium levels.
Phosphate
Renal failure (in renal osteomalacia)
X-ray usually of radius / ulnar
Diagnosis cannot be made with X-ray alone also need PHT and 25(OH)D level to rule out
other causes of demineralisation.
Rickets
Changes most easily seen at the ends of the radius and ulnar
Ragged bone edges
Apparent increased distance from arm bones to carpal bones (Due to
demineralisation of this area).
Fuzzy, cup-shaped diaphyses (ends of the bone)
General increase in radiolucency of the bone
Osteomalacia
Reduced amount of cortical bone
Partial fractures

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Treatment
Vitamin D supplements + calcium are first line 400U tablets, 1-2 times/day
After 3 weeks, x-ray improvements can be seen. Typically starting at the very tip of the
bone, and continuing down through the affected segment
Malapborption might require calciferol (1,25(OH)2D) - 1mg/day (equivalent to 40,000 units
of Vit D!)
Vit-D resistant rickets should be treated with calciferol 10,000 unites/day
Renal osteomalacia is best treated with alfacalcidol
Hypercalcaemia is common with all vit D treatments, especially alfacalcidol.

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