Rickets is a bone disorder where a baby’s growing bones don’t harden properly, leaving them soft and prone to deformity. It happens when a baby doesn’t have enough vitamin D, calcium, or phosphate to mineralize new bone tissue. The condition primarily affects the growth plates at the ends of long bones, which is why the legs, wrists, and ribs show the most visible changes. Rickets is preventable and treatable, but if missed, it can cause lasting skeletal problems.
How Rickets Develops in Growing Bones
A baby’s bones grow through a process where cartilage at the ends of long bones is gradually replaced by hard bone tissue. Cartilage cells mature, produce a soft framework called osteoid, and then calcium and phosphate crystals are deposited into that framework to make it rigid. This is what gives bone its strength.
When vitamin D, calcium, or phosphate levels are too low, that final hardening step fails. The soft osteoid keeps accumulating without ever becoming true bone. At the growth plates, cartilage cells pile up instead of being replaced, causing the ends of bones to widen and become disorganized. This is why a baby with rickets develops visibly thickened wrists and ankles, and why X-rays show characteristic changes at those sites.
Vitamin D plays a central role because it controls how well the gut absorbs calcium from food. Without enough vitamin D, calcium absorption drops. The body responds by pulling calcium from bones and flushing phosphate through the kidneys, which only worsens the mineral shortage at the growth plates.
What Causes It
The vast majority of infant rickets cases are nutritional, caused by not getting enough vitamin D. Breast milk, despite its many benefits, typically does not provide adequate vitamin D on its own. Babies who are exclusively breastfed without a vitamin D supplement are the group at highest risk.
Several factors increase that risk further. Babies born to mothers who were vitamin D deficient during pregnancy start life with lower stores. Maternal deficiency is strikingly common: studies have found rates of 18% in pregnant women in the UK, 42% in northern India, and 60 to 84% in non-Western women in the Netherlands. The vitamin D a baby is born with comes almost entirely from the mother, so a deficient mother nearly always means a deficient newborn. In rare cases of severe maternal deficiency, rickets can even begin in the womb.
Skin pigmentation matters too. Darker skin requires up to 10 times more sun exposure to produce the same amount of vitamin D as lighter skin. Families living at higher latitudes, in areas with heavy air pollution, or in cultures where clothing covers most of the body face additional risk because UV exposure drives the body’s own vitamin D production.
A small number of cases are genetic rather than nutritional. Some babies inherit conditions that cause the kidneys to waste phosphate, or that prevent the body from activating or responding to vitamin D. These hereditary forms are rare (about 4 per 100,000 births for the phosphate-wasting type) and typically don’t respond to standard vitamin D supplements.
Signs to Recognize
Rickets can be subtle in the earliest stages. One of the first physical signs a doctor may notice is craniotabes, a softening of the skull bones that makes parts of the baby’s head feel like a ping-pong ball when gently pressed. The soft spot on top of the head (fontanelle) may also be slow to close.
As the condition progresses, more visible signs emerge:
- Swollen wrists and ankles from widening of the growth plates
- Rachitic rosary, a row of bony bumps along the rib cage where the ribs meet the cartilage of the breastbone
- Frontal bossing, a prominent, squared-off forehead
- Breastbone projection, where the chest pushes forward
- Bowed legs or knock-knees, which develop once a child begins weight-bearing
- Delayed tooth eruption
- Bone pain and general fussiness
When blood calcium drops significantly, babies can develop tight muscle tone, irregular breathing patterns, and in serious cases, seizures. These are signs of dangerously low calcium rather than the bone disease itself, but they often occur together.
How Rickets Is Diagnosed
Doctors use a combination of blood tests and X-rays. Blood work typically checks vitamin D levels, calcium, phosphate, parathyroid hormone, and an enzyme called alkaline phosphatase (ALP). ALP is normally found in the range of 30 to 120 IU/L in a standard lab reference, but in babies with rickets caused by calcium or vitamin D deficiency, ALP can soar to 2,000 IU/L. That dramatic elevation is a strong signal that bone turnover is abnormal.
X-rays of the wrists or knees are the most reliable confirmation. The earliest change visible on an X-ray is widening of the growth plate, reflecting new cartilage forming without being converted to bone. As rickets advances, the ends of the long bones develop a characteristic “cupped” and “frayed” appearance, meaning the normally smooth, crisp bone edges become ragged and scooped out. These changes are most obvious at the wrists, knees, and along the ribs.
Treatment and Recovery
Nutritional rickets is treated with vitamin D supplementation at doses much higher than the daily prevention amount. For babies between 1 and 12 months, treatment doses typically range from 1,000 to 5,000 IU daily, compared to the 400 IU used for prevention. Calcium intake also needs to be adequate, around 1,000 mg per day, to supply the minerals the healing bones need. Without enough calcium during treatment, a phenomenon called “hungry bone syndrome” can occur, where the recovering bones absorb calcium so rapidly that blood calcium levels actually drop further.
With proper treatment, blood chemistry usually begins improving within weeks, and X-ray changes start to resolve over a few months. Most babies with nutritional rickets recover fully if treatment starts early. Mild bowing of the legs often corrects itself as the child grows.
Genetic forms of rickets require specialized treatment. Phosphate-wasting conditions need phosphate supplements and sometimes activated forms of vitamin D. Some inherited types don’t respond to vitamin D at all, which is why doctors investigate the underlying cause rather than simply prescribing supplements when a baby doesn’t improve as expected.
What Happens if Rickets Goes Untreated
Left untreated, rickets leads to progressive bone deformities that can become permanent. Severe bowing of the legs or knock-knees may eventually require corrective surgery. Growth can be stunted because the growth plates aren’t functioning normally. Dental problems are common, including delayed eruption and weakened enamel. Seizures from low calcium are the most dangerous acute complication and can occur without much warning in a baby who otherwise seems only mildly affected.
Prevention
The CDC recommends that all babies under 12 months receive 400 IU of vitamin D daily. Babies who are exclusively breastfed, or who get a mix of breast milk and formula, need a daily vitamin D supplement to reach that amount. Babies fed only infant formula do not need a separate supplement, because formula is already fortified with vitamin D.
For mothers, maintaining adequate vitamin D during pregnancy helps ensure the baby is born with reasonable stores. This is especially important for women with darker skin, limited sun exposure, or who live in northern climates. Checking vitamin D levels during pregnancy is increasingly common and gives mothers a chance to correct a deficiency before it affects the baby.