- Bone is composed of both cells and matrix
- Also contains blood vessels, nerves and haemopoeitic system
- Bones cells
- Osteoblasts are responsible for bone formation
- Osteoclasts are responsible for bone resorption
- Serum alkaline phosphatase reflects osteoblastic activity
- Matrix
- Has both mineralised and unmineralised components
- Mineralised component is made up of hydroxyapatite
- Osteoid is the unmineralised component
- Made up of 90% collagen and 10% non-collagenous proteins
- Non-collagenous proteins include proteoglycans and glycoproteins
Calcium homeostasis
- 98% of bodies calcium is stored within the skeleton
- At homeostasis turnover results in equal flux in and out of skeleton
- Calcium homeostasis is maintained by parathyroid hormone, Vitamin D3 and calcitonin
Parathyroid hormone
- 84 amino acid protein produced by parathyroid glands
- Increases serum calcium
- Increases renal calcium reabsorption
- Increases skeletal turnover
- Increases renal production of dihydroxy-vitamin D3
Cholecalciferol
- Is vitamin D3
- Under normal circumstances is produced in the skin by action of sunlight on precursors
- Hydroxylated in the liver to 25-hydroxy-vitamin D3
- Hydroxylated in kidney to 1,25 dihydroxy-vitamin D3
- Increases renal reabsorption of calcium
- Increases gastrointestinal absorption of calcium
- Increases skeletal calcium resorption
Calcitonin
- Produced by thyroid parafollicular C cells
- Reduces serum calcium
- Inhibits bone calcium resorption
Osteomalacia and rickets
- Vitamin D deficiency results in incomplete osteoid mineralisation
- In childhood, prior to epiphyseal closure, causes rickets
- In adults causes osteomalacia
Causes
- Vitamin D deficiency
- Malabsorption
- Post-gastrectomy or bowel resection
- Coeliac disease
- Cirrhosis
- Renal disease
- Renal tubular disorder (e.g. familial hypophosphataemic rickets)
- Chronic renal failure
- Anticonvulsant therapy
- Tumours
Clinical features
- Osteomalacia usually due to dietary deficiency in the elderly or Asian population
- Rickets usually due to familial hypophosphataemic rickets
- Rickets usually presents in early childhood with
- Failure to thrive
- Valgus or varus long bone deformities
- Skull deformities = craniotabes
- Enlarged costochondral junctions = Rickety rosary
- Lateral indentation of the chest wall = Harrison's sulcus
- X-ray shows widened epiphyses and cupped distal metaphysis
- Osteomalacia presents with
- Bone pain and tenderness
- Proximal myopathy
- True pathological or pseudo-fractures
- X-ray shows translucent bands in medical femoral cortex, pubic ramus or scapula
-
= Looser's zones
- In osteomalacia
- Serum calcium and phosphate are low
- Alkaline phosphatase is increased
- In familial hypophosphataemic rickets
- Serum calcium is normal and phosphate is low
- Bone biopsy would show increased unmineralised osteoid
Treatment
- Vitamin D replacement therapy
- Phosphate supplements in familial hypophosphataemic rickets
Bibliography
Renton P. Radiology of rickets, osteomalacia and hyperparathyroidism. Hosp Med 1998; 59: 399-403.
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