Here is a discussion of Osteomalacia regarding its definition, causes, pathogenesis, clinical pictures, investigations and treatment .
• Osteomalacia is characterized by defective bone mineralization, bone pain, muscle weakness and pathological fractures.
• There is failure to replace the turn over of Ca and P in bone matrix ===> bone become demineralised and the bony substance becomes replaced by soft osteoid tissue so it is mainly a qualitative bone defect.
The most common cause is vitamin D deficiency, the low levels of vitamin D causes a reduction of calcium absorption from the intestine.
The low calcium absorption stimulates parathyroid hormone secretion which restores serum calcium levels towards normal by increasing bone resorption and renal tubular calcium reabsorption. The level of parathyroid hormone also promotes phosphaturia and causes phosphate depletion. It is the combination of
calcium loss from bone and phosphate depletion that leads to impaired bone mineralization .
- Dietary decreased intake
- Lack of synthesis in skin.
- Decreased absorption.
- Defective metabolism
- Anticonvulsants
- Chronic Renal Failure CRF
• Low P with normal vit.D
- Familial hypophosphatemic rickets.
- Renal tubular disease.
• ·Osteomalacia with normal Ca, P and vit.D
- Hypophosphatasia
- Fibrogenesis imperfecta.
- Aluminium bone disease.
• Bone tenderness . Tetany may be manifested.
• Muscular weakness with marked proximal myopathy with waddling gait.
(Osteomalacia is the adult counterpart of rickets).
• Alkaline phosphatase : ++ , parathyroid hormone: ++ , Low vitamin D level.
• X ray : bone rarefaction with translucent band (pseudofraction or looser's zones) i.e linear areas of low density surrounded by sclerotic borders.
• Vit. D, Ca supplements.
• Diet e.g milk, cheese or yoghurt
• Alfacalcidol especially in cases of renal failure.
• Osteomalacia is characterized by defective bone mineralization, bone pain, muscle weakness and pathological fractures.
• There is failure to replace the turn over of Ca and P in bone matrix ===> bone become demineralised and the bony substance becomes replaced by soft osteoid tissue so it is mainly a qualitative bone defect.
How Osteomalacia develops ?
Pathogenesis of OsteomalaciaThe most common cause is vitamin D deficiency, the low levels of vitamin D causes a reduction of calcium absorption from the intestine.
The low calcium absorption stimulates parathyroid hormone secretion which restores serum calcium levels towards normal by increasing bone resorption and renal tubular calcium reabsorption. The level of parathyroid hormone also promotes phosphaturia and causes phosphate depletion. It is the combination of
calcium loss from bone and phosphate depletion that leads to impaired bone mineralization .
Causes of osteomalacia
• Vit. D deficiency- Dietary decreased intake
- Lack of synthesis in skin.
- Decreased absorption.
- Defective metabolism
- Anticonvulsants
- Chronic Renal Failure CRF
• Low P with normal vit.D
- Familial hypophosphatemic rickets.
- Renal tubular disease.
• ·Osteomalacia with normal Ca, P and vit.D
- Hypophosphatasia
- Fibrogenesis imperfecta.
- Aluminium bone disease.
Clinical picture
• Skeletal discomfort (from bone and muscle pain).• Bone tenderness . Tetany may be manifested.
• Muscular weakness with marked proximal myopathy with waddling gait.
(Osteomalacia is the adult counterpart of rickets).
Investigations to diagnose Osteomalacia
• Serum Ca : Low . Serum P : Low but ++ in CRF• Alkaline phosphatase : ++ , parathyroid hormone: ++ , Low vitamin D level.
• X ray : bone rarefaction with translucent band (pseudofraction or looser's zones) i.e linear areas of low density surrounded by sclerotic borders.
Treatment of Osteomalacia
• Treatment of the cause.• Vit. D, Ca supplements.
• Diet e.g milk, cheese or yoghurt
• Alfacalcidol especially in cases of renal failure.