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PH-MS11

Osteomalacia, rickets and other metabolic bone disease

Why bone matrix fails to mineralise when vitamin D, calcium or phosphate runs short, how that softens adult bone (osteomalacia) and disorganises the growth plate (rickets), how kidney disease remodels bone, and why scurvy is a matrix defect.

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  • 5 steps · 10 questions
  • 3D anatomy, affected parts marked

By the end, you can

  • Explain how bone matrix is laid down and mineralised, and what mineralisation needs from vitamin D, calcium, phosphate and the kidney.
  • Compare calcipenic and phosphopenic causes of defective mineralisation and predict their blood results.
  • Relate wide osteoid seams, Looser zones and a failing growth plate to the symptoms and deformities of osteomalacia and rickets.
  • Describe renal osteodystrophy as a spectrum of high and low bone turnover, with hyperparathyroid bone disease as the high-turnover comparison.
  • Distinguish disorders of bone mass, mineral and matrix (osteoporosis, osteomalacia, scurvy), and explain the main tests and how each treatment acts on the mechanism.

What it is

Osteomalacia is defective mineralisation of newly formed bone matrix (osteoid) in adults, so bone becomes soft; rickets is the same defect in a growing child, where it also affects the cartilage of the growth plates. Most cases are calcipenic (too little vitamin D or calcium) or phosphopenic (the kidney wastes phosphate). Renal osteodystrophy is the bone disease of chronic kidney disease; scurvy is a defect of the collagen matrix itself.

4 types to tell apart
Calcipenic osteomalacia and rickets
Vitamin D deficiency, very low calcium intake, malabsorption or inherited faults in making or sensing calcitriol; secondary hyperparathyroidism lowers phosphate.
Phosphopenic osteomalacia and rickets
Renal phosphate wasting, usually from excess FGF23 (X-linked hypophosphataemia, tumour-induced osteomalacia) or proximal tubule damage (Fanconi syndrome); calcium and PTH are usually normal.
Renal osteodystrophy
The bone component of CKD–mineral and bone disorder: high-turnover osteitis fibrosa, low-turnover adynamic bone disease, osteomalacia or a mixture.
Scurvy
Vitamin C deficiency: collagen cannot be stabilised, so too little sound matrix is made and vessels bleed.

US spelling: fibres → fibers.

Normal function

Matrix first, then mineral

Bone is built in two steps. Osteoblasts first secrete osteoid, an unmineralised matrix made mostly of type I collagen. Over the following days to weeks, calcium and phosphate crystallise between the collagen fibres as hydroxyapatite. Osteoblasts make alkaline phosphatase, which breaks down pyrophosphate, a natural inhibitor of crystal growth. Because mineralisation normally keeps pace, only thin seams of fresh osteoid are seen on bone surfaces, and every lamella of the and is mineralised.

The two components do different jobs, like steel rods in concrete: collagen resists stretching and bending, mineral makes bone stiff and hard. Mineral supply depends on the blood: enough calcium and phosphate must be present together. Vitamin D made in the skin by sunlight, or eaten, is converted by the liver to 25-hydroxyvitamin D (the storage form, which is what blood tests measure) and by the kidney to calcitriol, which raises gut absorption of calcium and phosphate. The proximal tubule reabsorbs filtered phosphate; PTH and FGF23, a hormone from , make it excrete more.

In children, long bones lengthen at the growth plates. Chondrocytes multiply in columns, enlarge (the hypertrophic zone), calcify the cartilage around them and die; vessels then invade, and osteoblasts lay bone on the calcified cartilage scaffold. In the usual explanation, hypertrophic chondrocytes need enough phosphate to complete this programme, so the growth plate is very sensitive to a mineral shortage.

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