Osteomalacia

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Osteomalacia is the softening of the bones caused by defective bone mineralization secondary to inadequate amounts of available phosphorus and calcium, or because of overactive resorption of calcium from the bone as a result of hyperparathyroidism (which causes hypercalcemia, in contrast to other aetiologies).[1] 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. It may show signs as diffuse body pains, muscle weakness, and fragility of the bones. The most common cause of the disease is a deficiency in vitamin D, which is normally obtained from the diet and/or from sunlight exposure.[2]

General characteristics

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.

Causes

The causes of adult osteomalacia are varied, but ultimately result in a vitamin D deficiency:

Signs and Symptoms

  • Weak bones
  • Bone pain
  • Muscle weakness
  • Hypocalcemia
  • Compressed vertebrae
  • Pelvic flattening
  • Easy fracturing
  • Bone softening
  • Bending of bones

Clinical features

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[6] 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.

It differs from renal osteodystrophy, where the latter shows hyperphosphatemia.

Biochemical findings

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 are given below:

  • The serum calcium is low
  • Urinary calcium is low
  • Serum phosphate is low except in cases of renal osteodystrophy
  • Serum alkaline phosphatase is high

Furthermore, a technetium bone scan will show increased activity.

Template:Bone pathology

Radiographic characteristics

Radiological appearances include:

Treatment

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[7] of significant amounts of vitamin D.

References

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See also

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  1. TheFreeDictionary > osteomalacia Citing: Mosby's Medical Dictionary, 8th edition. Copyright 2009
  2. MedlinePlus Medical Encyclopedia: Osteomalacia
  3. "Autoimmunity research foundation, Science behind Vitamin D". Retrieved 2011-07-19.Page Module:Citation/CS1/styles.css must have content model "Sanitized CSS" for TemplateStyles (current model is "CSS").

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