Vitamin D is primarily supplied through food—mainly of animal origin—or produced in the skin from 7-dehydrocholesterol under the influence of sunlight. This process is closely related to one’s place of residence and may be inefficient due to varying sunlight exposure in different countries, as well as the presence of smoke and dust in large cities, which absorb solar radiation. Commonly used UV filters also effectively block the natural synthesis of vitamin D3 in the skin.
In a child’s body, regardless of its source, vitamin D undergoes enzymatic transformation in the liver and kidneys into its active form—calcitriol. This compound activates the synthesis of a specific transport protein that facilitates the absorption of calcium from food through the intestinal wall and ensures proper bone mineralization.
There are many factors that can lead to the development of rickets.
In rickets caused by vitamin D3 deficiency, the main factor is its insufficient supply during periods of rapid weight gain in infancy, early childhood, and adolescence. Diseases associated with malabsorption syndrome, or impaired kidney and liver function, may also lead to vitamin D deficiency despite adequate intake. A similar effect can result from an improper diet—for example, overfeeding children with cow’s milk or excessive consumption of oatmeal, groats, or flour. These foods contain phytin, which forms insoluble complexes with calcium in the intestines, preventing its absorption.
Good sources of vitamin D include liver, egg yolks, butter, cream, cod liver oil, and fatty fish (sardines, mackerel, herring, salmon, tuna), as well as vitamin D–fortified infant milk formulas.
Other factors affecting calcium deficiency in a child’s body include genetic sensitivity to vitamin D3, the aforementioned environmental factors, and the use of certain medications, such as anticonvulsants.
Symptoms of Rickets
The first, so-called early (prodromal) symptoms of rickets observed in infants between the 2nd and 3rd month of life include irritability, restlessness, sleep disturbances, sweating of the head during feeding, frequent head movements, poor appetite, and related growth stagnation.
Early skeletal symptoms include:
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Softening and flattening of the occiput (the back of the head), which bends under pressure like parchment or a ping-pong ball.
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Enlargement or delayed closure of the anterior fontanelle.
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Chest deformities (bell-shaped chest, Harrison’s groove).
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The so-called “rachitic rosary”—thickening of the costochondral junctions of the ribs.
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“Frog belly”—a large, protruding abdomen caused by weak muscle tone.
The full development of untreated rickets usually occurs between the 3rd and 6th month of life, and the most pronounced deformities—especially of the lower limbs—appear toward the end of the 1st and during the 2nd year of life. These include:
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Further skull deformities (prominent forehead, squared skull).
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Chest deformities, with flattened sides and a protruding sternum (pigeon chest).
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Formation of “rachitic bracelets”—thickened wrist bones.
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Spinal curvature—so-called rachitic hump.
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Deformities of the lower limbs, appearing when the child begins to walk: bowlegs (O-shaped) or knock-knees (X-shaped).
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Flat feet.
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Pelvic deformities, resulting in flattening.
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Growth retardation and delayed motor development—the child sits, stands, and walks later than peers.
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Anaemia and recurrent respiratory infections are also more common.
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Dental abnormalities, such as open bite, narrow upper jaw, and high-arched (“gothic”) palate. Delayed tooth eruption, enamel defects, and cavities are also characteristic.
Diagnosis is based primarily on a detailed analysis of lifestyle, medical history, diet, medications, vitamin D3 supplementation, and characteristic clinical features.
Treatment
Rickets often resolves spontaneously around the age of two, as diet changes, growth slows, and the child spends more time in the sun. However, existing bone deformities are difficult—or sometimes impossible—to correct, and poorly mineralized bones remain more prone to fractures later in life. It should be noted that rickets may reappear during adolescence in rapidly growing youths.
Treatment of symptomatic rickets must always be supervised by a doctor. It involves changing the daily dose of vitamin D3 from a preventive to a therapeutic one. Self-treatment is strongly discouraged, as excessive intake of vitamin D can easily lead to overdose and serious side effects.
Prevention
Prevention of rickets begins during pregnancy. The expectant mother should, in addition to maintaining a balanced diet and spending time in sunlight, take vitamin D3 supplements, especially in the third trimester.
A newborn is born with vitamin D reserves, which depend on the mother’s diet during pregnancy. These reserves are usually depleted by the end of the first month of life. Therefore, it is advisable to begin preventive measures early—taking the baby for regular walks in daylight and administering vitamin D3 supplements as recommended.
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