|Classification and external resources|
Osteomalacia is the softening of the bones caused by defective bone mineralization secondary to inadequate levels of available phosphate and calcium, or because of overactive resorption of calcium from the bone as a result of hyperparathyroidism (which causes hypercalcemia). Osteomalacia in children is known as rickets, and because of this, use of the term "osteomalacia" is often restricted to the milder, adult form of the disease. Signs and symptoms can include diffuse body pains, muscle weakness, and fragility of the bones.
The most common cause of osteomalacia is a deficiency in vitamin D, which is normally derived from sunlight exposure and, to a lesser extent, from the diet. Nursing home residents (and the elderly in general) are at particular risk for vitamin D deficiency, as both the efficiency of vitamin D synthesis in the skin and the absorption of vitamin D from the intestine decline with age. The most specific screening test for vitamin D deficiency in otherwise healthy individuals is a serum 25(OH)D level.
Measures to prevent and treat osteomalacia revolve around intake of vitamin D and calcium supplements. Vitamin D should always be repleted in conjunction with calcium supplementation since most of the consequences of vitamin D deficiency are a result of impaired mineral ion homeostasis.
Osteomalacia is a generalized bone condition in which there is inadequate mineralization of the bone. Many of the effects of the disease overlap with the more common osteoporosis, but the two diseases are significantly different. There are two main causes of osteomalacia: (1) insufficient calcium absorption from the intestine because of lack of dietary calcium or a deficiency of, or resistance to, the action of vitamin D; and (2) phosphate deficiency caused by increased renal losses.
Osteomalacia is derived from Greek: osteo- which means "bone", and malacia which means "softness". In the past, the disease was also known as malacosteon and its Latin-derived equivalent, mollities ossium. Osteomalacia is associated with increase in osteoid maturation time.
The causes of adult osteomalacia are varied, but ultimately result in a vitamin D deficiency:
- Insufficient nutritional quantities or faulty metabolism of vitamin D or phosphorus
- Renal tubular acidosis
- Malnutrition during pregnancy
- Malabsorption syndrome
- Chronic renal failure
- Tumor-induced osteomalacia
- Long-term anticonvulsant therapy
- Coeliac disease
- Cadmium poisoning, Itai-itai disease
Signs and Symptoms
- Weak bones
- Bone pain
- Spinal bone pain
- Pelvic bone pain
- Leg bone pain
- Muscle weakness
- Compressed vertebrae
- Pelvic flattening
- Easy fracturing
- Bone softening
- Bending of bones
Osteomalacia in adults starts insidiously as aches and pains in the lumbar (lower back) region and thighs, spreading later to the arms and ribs. The pain is symmetrical, non-radiating and is accompanied by sensitivity in the involved bones. Proximal muscles are weak, and there is difficulty in climbing up stairs and getting up from a squatting position.
Due to demineralization bones become less rigid. Physical signs include deformities like triradiate pelvis and lordosis. The patient has a typical "waddling" gait. However, those physical signs may derive from a previous osteomalacial state, since bones do not regain their original shape after they become deformed.
Pathologic fractures due to weight bearing may develop. Most of the time, the only alleged symptom is chronic fatigue, while bone aches are not spontaneous but only revealed by pressure or shocks.
Biochemical features are similar to those of rickets. The major factor is an abnormally low vitamin D concentration in blood serum.
Major typical biochemical findings include:
- Low serum and urinary calcium
- Low serum phosphate, except in cases of renal osteodystrophy
- Elevated serum alkaline phosphatase (due to an increase in compensatory osteoblast activity)
- Elevated parathyroid hormone (due to low calcium)
Furthermore, a technetium bone scan will show increased activity (also due to increased osteoblasts).
|Condition||Calcium||Phosphate||Alkaline phosphatase||Parathyroid hormone||Comments|
|Osteoporosis||unaffected||unaffected||normal||unaffected||decreased bone mass|
|Osteopetrosis||unaffected||unaffected||elevated||unaffected||thick dense bones also known as marble bone|
|Osteomalacia and rickets||decreased||decreased||elevated||elevated||soft bones|
|Osteitis fibrosa cystica||elevated||decreased||elevated||elevated||brown tumors|
|Paget's disease of bone||unaffected||unaffected||variable (depending on stage of disease)||unaffected||abnormal bone architecture|
Radiological appearances include:
Nutritional osteomalacia responds well to administration of 10,000 IU weekly of vitamin D for four to six weeks. Osteomalacia due to malabsorption may require treatment by injection or daily oral dosing of significant amounts of vitamin D.
- TheFreeDictionary > osteomalacia Citing: Mosby's Medical Dictionary, 8th edition. Copyright 2009
- MedlinePlus Medical Encyclopedia: Osteomalacia
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- Osteopetrosis, the opposite of osteomalacia