Rickets and osteomalacia
- Lesion
Without enough vitamin D or phosphate, new bone matrix cannot harden. Children get bent bones and wide growth plates; adults get soft, painful bones.
What it is
Rickets (in children, before the growth plates close) and osteomalacia (in adults) are failures to mineralize newly made bone matrix. The usual cause is lack of vitamin D from poor sun exposure, diet or malabsorption, kidney or liver disease, but low phosphate states such as X-linked hypophosphatemic rickets and tumour-induced osteomalacia (FGF23 excess) produce the same picture. Excess unmineralized osteoid covers the trabeculae, bone softens and bends, and in children the growth plate becomes a wide, disorganized mass of cartilage.
Structure
- Trabeculae are covered by thick seams of pale pink unmineralized osteoid on H&E.
- Rickets growth plate: the zone of provisional calcification fails, hypertrophic chondrocytes pile up in irregular, elongated tongues and the metaphysis flares.
- Gross: soft bones bend under weight (bowed legs), the ribs bead at costochondral junctions and the pelvis may deform.
- Looser zones: bands of osteoid crossing the cortex, typically in the pubic rami, femoral neck and scapula.
Step by step
- Vitamin D comes from skin synthesis and diet and is activated by the liver (25-hydroxylation) and the kidney (1-alpha-hydroxylation).
- Active vitamin D increases intestinal absorption of calcium and phosphate.
- Deficiency lowers calcium and phosphate absorption; low calcium raises PTH.
- PTH keeps calcium near normal but wastes phosphate in the urine, so the calcium-phosphate product falls.
- Osteoblasts still lay down matrix, but it cannot mineralize: osteoid accumulates and bone softens.
Causes of defective mineralization
| Group | Examples | Laboratory pattern |
|---|---|---|
| Vitamin D lack | Little sun, dark skin at high latitude, exclusive breastfeeding without supplements, diet | Low 25-hydroxyvitamin D, high PTH, high alkaline phosphatase |
| Malabsorption | Celiac disease, pancreatic insufficiency, bariatric surgery, cholestasis | As vitamin D lack |
| Organ disease | Chronic kidney disease (no 1-alpha-hydroxylation), liver disease, anticonvulsants | Low calcitriol in kidney disease |
| Phosphate wasting | X-linked hypophosphatemic rickets, tumour-induced osteomalacia | Low phosphate, high FGF23, normal calcium |
| Vitamin D-dependent rickets | Defects of 1-alpha-hydroxylase or the vitamin D receptor | Low calcium; calcitriol low or very high |
Clinical notes
- Toddler with bowed legs, delayed walking, wide wrists and beaded ribs: nutritional rickets until shown otherwise.
- Adult with diffuse bone pain, waddling gait and proximal weakness: think of osteomalacia, especially after bariatric surgery or with malabsorption.
- Severe hypocalcaemia from rickets can cause tetany or seizures in infants.
Test yourself
Think of the answer, then tap the question to see it.
What is the basic defect in rickets and osteomalacia?
Failure to mineralize newly formed osteoid.
What is the rachitic rosary?
Bead-like swelling of the costochondral junctions from overgrown, unmineralized cartilage and osteoid.
What are Looser zones?
Pseudofractures: bands of unmineralized osteoid crossing the cortex in osteomalacia.
Which hormone is high in X-linked hypophosphatemic rickets?
FGF23, which makes the kidney waste phosphate and lowers calcitriol.
Elsewhere in DurgiPedia
Connections
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Rickets: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2025); Osteomalacia: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2025).
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Representative model, for educational purposes only.