X-ray of the legs in a two-year-old child with rickets
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Osteomalacia

Osteomalacia (pronounced /ˌɑstioməˈleɪʃiə/),is also referred to as bow-leggedness or rickets - taken from the Greek word ῥάχις (rhákis), meaning "spine". It is a disorder which relates directly to Vitamin D deficiency, which causes a lack of calcium being absorbed. Because calcium is an essential nutrient which aids bone rigidity, the lack of it being absorbed into the body causes fragile or malformed bones, which are unable to support the weight of a growing body. more...

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Although osteomalacia can occur in adults, the majority of cases occur in children with poor nutrient intake usually resulting from famine or starvation during early stages of childhood.

Aetiology

Vitamin D is created by the body when it is exposed to UV light, which is more commonly known as being present in sunlight. In 1916, German medical research scientist and pediatrician Kurt Huldschinsky (1883-1940) discovered that exposing patients who had osteomalacia to artificially generated ultra-violet light, or by therapeutically exposing them to sunlight, he was able to yield quicker recovery than other methods, such as supplementation of dairy products within a patient's diet.

Vitamin D3 is produced naturally by the human body on exposure to UVB in sunlight. Vitamin D is also added to milk, milk products, and multi-vitamin pills through a process originally patented by Harry Steenbock. Some people who do not get enough sun exposure, milk products, or green vegetables may also develop the disease. Deficiency of calcium can also cause rickets, particularly in some developing countries where the intake of calcium-rich products such as leafy greens, nuts, and seeds is low.

Hereditary rickets is caused by an inherited disease that interferes with phosphate absorption in the kidney or by Renal tubular acidosis, in which calcium is taken from the bones to counteract acid produced in the kidneys. Rickets can also be caused by certain liver diseases.

Manifestations of disease

Rickets causes bone pain, slowed growth in children, dental problems, muscle loss and increased risk of fractures (easily broken bones). Medical problems seen in children with rickets are

  1. Vitamin D deficiency,
  2. Skeletal deformity,
  3. Growth disturbance,
  4. Hypocalcaemia (low level of calcium in the blood),
  5. Tetany (uncontrolled muscle spasms).

The X-ray, or radiograph, in the article is the classic image of advanced rickets sufferers: bow legs (outward curve of long bone of the legs) and a deformed chest. Changes in the skull also occur causing a distinctive "square headed" appearance. These deformities persist into adult life.

Treatment and prevention

Treatment involves increasing dietary intake of calcium, phosphates and Vitamin D. Exposure to sunshine, cod liver oil, halibut-liver oil, and viosterol are all sources of vitamin D.

Rickets is a severe and prolonged vitamin D deficiency that leads to softening and weakening of the bones in children. Vitamin D helps the body absorb calcium and phosphate, which children need to build strong bones. Good sources of dietary vitamin D are vitamin D-fortified formulas and milk.

Read more at Wikipedia.org


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Vitamin D and bone mineral density status of healthy school children
From Nutrition Research Newsletter, 9/1/05 by R. Marwaha

Vitamin D status has a profound effect on the growth and development of children and has major implications for adult bone health. Overt cases of vitamin D deficiency represent only the tip of an iceberg of vitamin D insufficiency. Whereas severe vitamin D deficiency, usually associated with 25-hydroxyvitamin D [25(OH)D] concentrations <5.0 ng/mL, results in rickets and osteomalacia, even less severe deficiency has been associated with numerous negative skeletal consequences, including secondary hyperparathyroidism, increased bone turnover, enhanced bone loss, and fracture risk.

In assessing a person's vitamin D status, because 1,25-dihydroxyvitamin D [1,25[(OH).sub.2]D] can be normal, high, or low in vitamin D deficiency, the most commonly used and most sensitive index is 25(OH)D. Age, sex, pubertal status, latitude, season, race, and ethnicity influence serum concentrations of 25(OH)D. The objectives of the current study were to assess the prevalence of clinical and biochemical vitamin D deficiency in healthy children and adolescents aged 10 y to 18 y during their period of most rapid growth, to compare the biochemical variables of the calcium-vitamin D axis between 2 socioeconomic groups, and to study the effect of hypovitaminosis D on BMD.

The study was conducted in 5137 apparently healthy schoolchildren (aged 10 y to 18 y) of both sexes in urban New Delhi, India. The children attended 2 state-run schools that catered to children of lower socioeconomic status (LSES) and 2 private schools that enroll children of upper socioeconomic status (USES). Socioeconomic stratification of the subjects was based on the type of school attended. Of the above 5137 subjects, 3089 (1079 boys, 2010 girls) from state-run schools made up the LSES group, and 2048 (968 boys, 1080 girls) from private schools made up the USES group. The subjects were further divided into 3 age groups: 10 y old to 12 y old, 13 y old to 15 y old, and 16 y old to 18 y old.

This entire cohort of 5137 children and adolescents underwent clinical examination and anthropometric assessment, including a recording of the stigmata of vitamin D deficiency. A sunlight exposure questionnaire was administered to each child. Clinical vitamin D deficiency was diagnosed if a subject had either genu varum (bowlegs) or genu valgum (knock-knees). Of this large cohort, 760 children (430 from LSES and 330 from USES groups) selected by randomization from each class of the school underwent further laboratory assessment. Each class was divided into four groups according to the number of sections in the class, and all children from one randomly selected section (cluster) were called for blood sampling the next day. Dietary assessment of total energy, protein, carbohydrate, fat, calcium, and phytate was done in 349 subjects randomly selected from the cohort of 760 (171 from the LSES and 178 from the USES groups) through a 24-hour recall of their food intake.

A total of 5137 children were examined, and a 10.8% prevalence of clinical evidence of vitamin D deficiency was noted in 556 children. Boys had a prevalence of 10.4% and girls had a prevalence of 11.1%, and there was no significant difference between the 2 groups. This study found that the LSES group adolescents had significantly lower mean 25(OH)D concentrations than did the USES group adolescents. The only other study that compared low and high socioeconomic status groups did not find any significant difference in mean vitamin D concentration between the two groups. However, the difference that these researchers found is further supported by the observation that LSES group children also had higher iPTH, higher AP, and lower serum phosphorus concentrations than did USES group children. Because serum calcium concentration and sunlight exposure did not differ significantly between the two groups and because dietary calcium intake was significantly lower in the LSES group than in the USES group, nutrition may play an important role, as was reported earlier.

Children in the LSES group had significantly lower BMD values at the forearm than did those in the USES group. This difference could be due to poor overall nutrition, as evidenced by low BMIs, low dietary calcium intakes, low serum 25(OH)D concentrations, and secondary hyperparathyroidism. The researchers conclude that there is a high prevalence of clinical and biochemical hypovitaminosis D in apparently healthy schoolchildren in India. The observation that children from low socioeconomic backgrounds have significantly higher prevalences of vitamin D deficiency and low BMD suggests that nutrition plays an important role in the causation of hypovitaminosis D.

R. Marwaha, N. Tandon, D. Reddy, H. Reddy, et al. Vitamin D and bone mineral density status of healthy schoolchildren in northern India. AJCN; 82(2):477-482 (August 2005) [Correspondence: RK Marwaha, Department of Endocrinology and Thyroid Research, Institute of Nuclear Medicine and Allied Sciences, Timarpur, New Delhi 110054, India. E-mail: marwaharaman@hotmail.com]

COPYRIGHT 2005 Frost & Sullivan
COPYRIGHT 2005 Gale Group

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