Rickets is a childhood condition caused by serious vitamin D deficiency. This lacking in vitamin D results in weak, soft bones, along with slowed growth and skeletal development. Rickets is, by definition, a disorder which begins in childhood. If this problem occurs only later in life it is known as osteomalacia.
Rickets occurs when the body has a severe lack of vitamin D during the developmental years. Vitamin D is essential to the development of strong, healthy bones. A child with rickets can experience stunted growth and will most likely be short in stature as an adult. This is because, without proper vitamin D levels, decreased mineralization of the bones at the growth plate level affects the strength, size and shape of the bones. A related condition called osteomalacia can occur in adults with the same sort of vitamin D deficiency, but osteomalacia occurs only in adulthood after the growth plates of the bones have closed.
Most vitamin D is produced by the body, although some can be directly supplied by diet. In order to accomplish production of vitamin D, the body requires both cholesterol and ultraviolet light. Most often, the cholesterol comes from digesting animal tissue, oils, fats, and egg yolks. The ultraviolet light is usually supplied by direct sunlight. Only when this light is available can the skin alter the cholesterol molecule to make vitamin D. Children who do not receive enough sunlight are at greater risk of developing rickets, as are children with darker skin, which can block the ultraviolet rays. Vitamin D is found naturally in the foods listed above, but more often children receive vitamin D supplements through foods which have had the vitamin added, as in milk or infant formula.
Vitamin D is necessary in the body, because it can be converted into a hormone which stimulates calcium intake by the intestines. This conversion begins in the liver, where vitamin D becomes a hormone called 25-OH-D, and is completed when the kidneys convert 25-OH-D into a hormone called 1,25-diOH-D. This is the hormone that causes the intestines to absorb calcium from the person's diet. Without proper levels of vitamin D, there is not enough 1,25-diOH-D produced, which results in lower levels of calcium in the body. Adequate calcium is needed by the bones for both development and maintenance.
Causes and symptoms
Rickets is directly caused by insufficient calcium for bone mineralization during growth and development. This is caused by vitamin D deficiency which can be a result of too little cholesterol, ultraviolet light, or vitamin D supplement. During the Industrial Revolution, rickets was quite common in cities because pollution in the air blocked much of the sunlight needed for vitamin D production in the body. There is also a hereditary type of rickets, called X-linked hypophosphatemia, that causes the kidneys bo be unable to retain phosphate.
The most commonly recognized symptoms of rickets occur in the arms and legs, where stress on the underdeveloped bones can cause bowing. Children with rickets may feel pain or tenderness in the bones of their arms, legs, spine, pelvis, and ribs. The skull may develop an odd or asymmetrical shape. Calcium levels in the blood will be low and overall growth is often impaired.
The initial approach to diagnosing rickets involves a musculoskeletal examination followed by an x ray is often. Affected children may have obviously widened spaces between their joints or bowing of the bones in their arms and legs. Some children may not experience normal dental development as well. A doctor may also assess levels of serum calcium, alkaline phosphatase and other indicator chemicals by using a blood test. While calcium levels can be normal or slightly low, alkaline phosphatase levels in a child with rickets can be high even compared to a normal adult. While x rays can prove misleading, diagnosis by chemical analysis is highly accurate.
The treatment for rickets primarily involves corrections of the conditions which led to the disorder. This can be as simple as a change in diet to include foods high in vitamin D such as milk, fish, or liver. Treatment might also mean a gradual increase in the amount sunlight received by the child. In more severe cases, bracing or surgery may be necessary to aid in the correction and repair of bones. Treatment is usually mild and bone deformities usually reduce over time.
There is currently little known about any alternative method for treating rickets. Treatments which involve raising vitamin D levels and ultraviolet light exposure are usually simple and effective.
Children with rickets are likely to suffer from stunted growth, bone abnormalities and bone pain, however these symptoms often disappear with treatment. In women, deformation of the pelvic bone structure can prevent vaginal childbirth later in life. Most deformities correct with growth when proper levels of vitamin D are restored and normal bone calcification is maintained.
Rickets caused by vitamin D deficiency is simple to prevent. Commercially available infant formula is usually fortified with more than enough vitamin D for infants. For parents who breastfeed their children, it is recommended by the U.S. Department of Health and Human Services that children also receive 400 international units (10 micrograms) of vitamin D supplement. This is because human breast milk contains little vitamin D. It is also important that children are allowed decent amounts of sunlight. As little as twenty minutes each day can be sufficient. For children living in cities, where pollution is likely to block ultraviolet light, and children with dark skin, which can block ultraviolet light, vitamin D supplement is especially important.
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25-hydroxy-vitamin D— This is the form of vitamin D that is measured in order to assess vitamin D deficiency.
Cholesterol— A fat-soluble steroid alcohol (sterol) found in animal fats and oils, and in egg yolks. The human body needs cholesterol to produce vitamin D.
Growth plate— The place in long bones where growth occurs during childhood.
International unit (IU)— A measurement of biological activity in which one IU is equal to one mg (milligram).
Mineralization— The process by which the body uses minerals to build bone structure.
X-linked hypophosphatemia,— A type of rickets caused by genetic factors which prevent the kidneys from retaining phosphate.
Rickets was once considered an extremely common disorder of childhood. The term itself is derived from the old English word for "twist," or "wrick," and throughout history children with rickets could be identified by their bowed legs and knock knees, which gave them a twisted appearance.
Rickets is caused by a deficiency in vitamin D . During growth, human bone is made and maintained by the interaction of calcium , phosphorus , and vitamin D. Calcium is deposited in immature bone (osteoid) in a process called calcification, which transforms immature bone into its mature and familiar form. However, in order to absorb and use the calcium available in food, the body needs vitamin D. In rickets, the lack of this important vitamin leads to low calcium, poor calcification, and deformed bones.
Vitamin D is the only vitamin that can be both acquired through food and made by the body itself. Although vitamin D can be absorbed through foods rich in animal fat , such as milk, cheese, fish, and meat, this absorption constitutes only about 10 percent of what the body needs in a single day. The remaining 90 percent is created by the body. Ultraviolet radiation from the sun converts 7-dihydrocholesterol in the skin to vitamin D3. This is then converted to the hormone calcitriol (the active form of vitamin D) in the kidney. Calcitriol allows absorption of calcium and phosphorus in the gut, primarily in the small intestine, and maintains the body's balance of calcium and phosphate through the kidney and bone. Without adequate vitamin D, the body can only absorb 10 to 15 percent of the calcium available in food. This balance of vitamin D, calcium, and phosphate is essential to the growth and maintenance of bones, especially in children. Deficiencies can also occur in elderly adults, a condition called osteomalacia .
Historically, rickets plagued the populations of European countries in the northern latitudes—at one time it was called "the English disease." During the Industrial Revolution and into the early 1900s, smog filled the developing cities of Europe, diminishing the amount of sunlight to which children were exposed and causing an epidemic of rickets. Some researchers estimate that prior to 1915, almost 85 percent of children in these industrialized areas of Europe and North America suffered from rickets. With research into the sources and function of vitamin D in the 1920s, however, the use of cod-liver oil, fortified cow's milk, and fortified formula virtually eliminated rickets in Europe and North America.
As vitamin D can either be consumed in small quantities through the diet or made in the skin, there are two main groups of risk factors for developing rickets. Dietary risk factors include diets low in vitamin D–rich foods, such as eggs, cow's milk, meat, and fish. Breast milk, a primary source of childhood nutrition , contains very little vitamin D, and infants who are exclusively breastfed are more likely to develop the disease. While human milk does contain sufficient amounts of calcium and phosphorus for an infant, its vitamin D content is only 4-60 IU/L (international units per liter), while the full-term infant requires approximately 400 IU daily. Infants and children who are not exposed to sunlight, like those in smog-filled cities or those who remain indoors or covered for cultural or religious reasons, are also at increased risk of developing rickets. In children with darkly pigmented skin, melanin acts in a similar way to block sunlight's ability to help the skin make vitamin D. Dark-skinned people require almost six times as much sunlight exposure to make the same amount of vitamin D as those with lighter skin.
Populations that remain at risk today include people with darkly pigmented skin, those who live in industrialized northern cities, and children in certain Arab countries where covering clothing and staying indoors during early childhood are cultural norms. Even in tropical and sunny climates, rickets remains a problem in dense city centers like Calcutta and Johannesburg, and it is still diagnosed in mostly African-American children in the United States. Children who consume vegetarian or vegan diets, as well as infants of lactating mothers who have chronically low levels of vitamin D, may also be at increased risk for rickets. Although rare, diets directly deficient in calcium and/or phosphorus may also lead to rickets.
One of the earliest signs of rickets in the infant is craniotabes (a softening of the skull) and delayed closing of the anterior fontanelle (the soft spot on the head). The infant's skull becomes large and thick (though soft), and muscle tone is poor. Poor calcification of osteoid at the ends of bones makes the bone spread in that area. At the ends of ribs, these splayed areas create a knobby-looking chain called the "rachitic rosary" on the front of the chest. In other areas, the pressure of a child's weight bends poorly mineralized bones, creating shortness, bow legs, and knock knees. Poor calcification also creates weakness, making bones prone to fracture. Children can also have delayed dentition , pelvic abnormalities, and enlarged joints, along with a curved spine and a forward projected breastbone. Rickets also lowers a child's immune defenses. For those with severe and untreated disease, bone bowing, short stature, and fractures can lead to long-term pain and immobility and require bracing and/or surgery.
Luckily, rickets is a very treatable and preventable disorder. Researchers have found that as little as twenty to thirty minutes of sun exposure per week in children in temperate climates is sufficient to maintain adequate levels of vitamin D in the blood. Other studies have found that oral supplements of 400 IU of vitamin D daily, often in the form of fish-liver oil, can prevent the disease in at-risk populations. Supplementation can also aid in the healing process. A single dose of 600,000 IU, or gradual treatment with 5,000–10,000 IU daily for two to three months, can be a sufficient treatment. And although some bony deformities may remain, many will repair themselves, and most growth parameters will return to near normal. Treatment can prevent grave complications, including developmental delays, waddling gait, and seizures.
Once a widespread scourge of childhood, rickets is now a preventable and treatable disease. It is necessary to understand the roles of vitamin D, calcium, and phosphorus in bone growth, as well as the mechanism of the disease in order to appropriately diagnose and treat it. When addressing the global impact of this disease, it is especially important to understand local environments, community diets, and cultural beliefs.
see also Calcium; Minerals; Osteomalacia; Osteopenia; Osteoporosis.
Seema P. Kumar Neelima Pania
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rick·ets / ˈrikits/ • n. [treated as sing. or pl.] Med. a disease of children caused by vitamin D deficiency, characterized by imperfect calcification, softening, and distortion of the bones typically resulting in bow legs.