Osteomalacia occurs due to the deficiency of which vitamin
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Osteomalacia occurs due to deficiency of Vitamin D. The word Osteomalacia means soft bones. The condition keeps your bones from mineralizing or hardening as they should. That makes them weak and more likely to bend and break.
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Osteomalacia is the softening of the bones caused by impaired bone metabolism primarily due to inadequate levels of available phosphate, calcium, and vitamin D, or because of resorption of calcium. The impairment of bone metabolism causes inadequate 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. Signs and symptoms can include diffuse body pains, muscle weakness, and fragility of the bones. In addition to low systemic levels of circulating mineral ions necessary for bone and tooth mineralization, accumulation of mineralization-inhibiting proteins and peptides (such as osteopontin and ASARM peptides) occurs in the extracellular matrix of bones and teeth, likely contributing locally to cause matrix hypomineralization (osteomalacia).[1][2][3][4][5]
The most common cause of osteomalacia is a deficiency of vitamin D, which is normally derived from sunlight exposure and, to a lesser extent, from the diet.[6] The most specific screening test for vitamin D deficiency in otherwise healthy individuals is a serum 25(OH)D level.[7] Less common causes of osteomalacia can include hereditary deficiencies of vitamin D or phosphate (which would typically be identified in childhood) or malignancy.
Vitamin D and calcium supplements are measures that can be used to prevent and treat osteomalacia. Vitamin D should always be administered in conjunction with calcium supplementation (as the pair work together in the body) since most of the consequences of vitamin D deficiency are a result of impaired mineral ion homeostasis.[8]
Nursing home residents and the homebound elderly population are at particular risk for vitamin D deficiency, as these populations typically receive little sun exposure. In addition, both the efficiency of vitamin D synthesis in the skin and the absorption of vitamin D from the intestine decline with age, thus further increasing the risk in these populations. Other groups at risk include individuals with malabsorption secondary to gastrointestinal bypass surgery or celiac disease, and individuals who immigrate from warm climates to cold climates, especially women who wear traditional veils or dresses that prevent sun exposure.[9]
Signs and symptoms :
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:
insufficient calcium absorption from the intestine because of lack of dietary calcium or a deficiency of, or resistance to, the action of vitamin D
phosphate deficiency caused by increased renal losses.
Causes
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
Hypophosphatemia[11]
Chronic kidney failure
Tumor-induced osteomalacia (Oncogenic osteomalacia)
Long-term anticonvulsant therapy[12]
Celiac disease[13]
Cadmium poisoning, itai-itai disease
prevention
Prevention of osteomalacia rests on having an adequate intake of vitamin D and calcium. Vitamin D3 Supplementation is often needed due to the scarcity of Vitamin D sources in the modern diet.[citation needed]
Treatment
Nutritional osteomalacia responds well to administration of 2,000-10,000 IU of vitamin D3 by mouth daily. Vitamin D3 (cholecalciferol) is typically absorbed more readily than vitamin D2 (ergocalciferol). Osteomalacia due to malabsorption may require treatment by injection or daily oral dosing[15] of significant amounts of vitamin D3.
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