Osteomalacia

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Overview
Osteomalacia is the defective uptake of minerals into the normal or overgrowing protein bone matrix. It is considered a secondary bone formation impairment. It can lead to increased bone softness and a curvature of the bone. Osteomalacia in children is known as rickets, and because of this, 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.

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 in vitamin D.

Osteomalacia is derived from Greek: osteo refers to 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
 * Therapy with Fumaderm

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. Pain is non-radiating, symmetrical, and accompanied by tenderness in the involved bones. Proximal muscles are weak, and there is difficulty in climbing up stairs and getting up from a squatting position. Physical signs include deformities like triradiate pelvis and lordosis. The patient has a typical "waddling gait". Pathologic fractures due to weight bearing may develop. Most of the time, the only alleged symptom is chronic fatigue and bone aches are not spontaneous but only revealed by pressure or shocks.

Biochemical findings
Biochemical features are similar to rickets.The major fact is a collapsed vitamine D rate in blood or serum.

X Ray
Radiological appearances include
 * Indistinct border to the medullary spongiosa
 * Thinning of the basal lamina and end plates
 * Loss of definition in the trabecular details
 * Separation of the compact bone layers
 * Pseudofractures
 * Protrusio acetabuli

Lack of Circulating Vitamin D

 * Anticonvulsant therapy
 * Chronic Liver Disease
 * Chronic Renal Failure
 * Exocrine pancreatic insufficiency
 * Faulty bile function
 * Gastrectomy
 * Insufficient sun exposure
 * Malnurishment in advanced age
 * Mesenchymal tumors
 * Nephrotic Syndrome
 * Prostate Cancer
 * Small intestine disease
 * Undernurishment
 * Vegetarian diet

Peripheral Resistance to Vitamin D

 * Anticonvulsant therapy
 * Chronic Renal Failure
 * Vitamin D dependent ricketts

Hypophosphatemia

 * Chronic Dialysis
 * Fanconi syndrome
 * Malabsorbtion
 * Malnutrition
 * Neurofibromatosis
 * Primary Hypoparathyroidism
 * Toxins
 * Tumor phosphaturia

Miscellaneous

 * Calcium deficiency
 * Calcification inhibitors
 * Chronic acidosis
 * Hypoparathyroidism
 * Renal transplantation

Treatment
Nutritional osteomalacia responds well to administration of 200000 IU weekly of vitamin D for 4 to 6 weeks, followed by a maintenance dose of 1600 IU daily or 200000 IU every 4 to 6 months.