osteomalacia

Osteomalacia term for the softening of the bones due to defective bone mineralization. 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. A common cause of the disease is a deficiency in vitamin D, which is normally obtained from the diet and/or sunlight exposure.^[1]

General characteristics

Osteomalacia in the adult is most commonly found in confined, dark-skinned, or diet-disbalanced subjects. Many of the effects of the disease overlap with the more common osteoporosis, but the two diseases are significantly different. Osteomalacia is specifically a defect in mineralization of the protein framework known as osteoid. This defective mineralization is mainly caused by lack of vitamin D, or faulty bodily utilization of vitamin D.

Osteomalacia is derived from Greek: osteo- means "bone", and malacia 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.

• Insufficient sunlight exposure, especially in dark-skinned subjects
• 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
• Therapy with Fumaderm
• Celiac disease[1]

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 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 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:

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

Furthermore, a technetium bone scan will show increased activity.

Radiographic characteristics

Radiological appearances include:

• Pseudofractures, also called Looser’s zones.
• Protrusio acetabuli, a hip joint disorder

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^[2] of significant amounts of vitamin D.

References

1. ^ MedlinePlus Medical Encyclopedia: Osteomalacia
2. ^ Eisman JA (1988). "Osteomalacia". Baillières Clin Endocrinol Metab 2 (1): 125–5. doi:10.1016/S0950-351X(88)80011-9. 

See also

• Osteopetrosis, the opposite of osteomalacia