Rickets is a childhood bone disorder in which bones become soft and weak, leading to deformities like bowed legs and stunted growth. It happens when a child’s body doesn’t have enough calcium or phosphate to properly harden (mineralize) growing bones. The most common cause is a lack of vitamin D, which the body needs to absorb calcium from food.
How Rickets Affects Growing Bones
Healthy bones form when calcium and phosphate combine into hard mineral crystals that deposit onto a flexible protein framework called collagen. This process is especially active at the growth plates, the soft cartilage zones near the ends of long bones where new bone is being built as a child grows taller.
Vitamin D plays a central role in this process. Its active form increases the absorption of calcium from the intestines, a step that becomes critical when a child’s diet is low in calcium. Without enough vitamin D, the body absorbs far less calcium than it needs. The result is a buildup of soft, unmineralized bone tissue beneath the growth plates. Over time, this makes bones pliable instead of rigid, and the growth plates themselves widen rather than converting into solid bone.
Causes Beyond Vitamin D Deficiency
Nutritional rickets, caused by too little vitamin D, calcium, or both, is by far the most common form. Risk factors include limited sun exposure (the skin produces vitamin D from sunlight), dark skin (which reduces vitamin D synthesis), exclusive breastfeeding without supplementation (breast milk contains very little vitamin D), and diets low in dairy or fortified foods.
Less commonly, rickets has genetic causes. The best known is X-linked hypophosphatemia, an inherited condition caused by mutations in the PHEX gene. These mutations lead to an overproduction of a protein called fibroblast growth factor 23, which disrupts how the kidneys and intestines handle phosphate. The result is chronically low blood phosphate levels and poorly mineralized bones, even when vitamin D intake is normal. Because the altered gene sits on the X chromosome, X-linked hypophosphatemia follows an X-linked inheritance pattern, meaning it can be passed from either parent but tends to affect boys and girls somewhat differently.
Other rare forms involve kidney disorders that cause phosphate wasting, or genetic defects in the enzymes that activate vitamin D within the body. These conditions produce the same skeletal problems as nutritional rickets but don’t respond to standard vitamin D supplementation alone.
Signs and Symptoms
Rickets predominantly affects the longer, faster-growing bones, so deformities tend to show up in the legs, wrists, and ribs. Common signs include:
- Bowed legs or knock-knees: the classic visible deformity, caused by soft leg bones bending under a child’s weight.
- Swollen wrists and ankles: widened growth plates create a noticeable thickening at the joints.
- Rachitic rosary: a row of bead-like bumps along the front of the rib cage where cartilage meets bone.
- Frontal bossing: a prominent, protruding forehead from softened skull bones.
- Craniotabes: soft, thin areas on the skull, most often felt in young infants.
- Delayed tooth eruption and dental problems.
- Bone pain and tenderness, particularly in the legs, pelvis, and spine.
- Poor growth: children with rickets are often shorter than expected for their age.
These changes develop gradually. A mild case might only show up as slightly widened wrists on an X-ray, while severe, prolonged rickets can cause dramatic leg bowing and significant short stature.
How Rickets Is Diagnosed
Diagnosis relies on a combination of physical examination, blood tests, and X-rays. On an X-ray of the wrist or knee, the hallmark findings are widening, fraying, and cupping of the metaphysis, the flared zone just below the growth plate. Instead of a clean, sharp line at the end of the bone, the edge looks ragged and irregular. These changes are most easily spotted at the wrists (the ends of the radius and ulna) and around the knees.
Blood tests help confirm the diagnosis and identify the underlying cause. A key marker is alkaline phosphatase, an enzyme released by bone-building cells. In nutritional rickets, levels can climb to five or even ten times the upper limit of normal. Calcium levels are often low (or low-normal), while phosphate levels tend to be decreased as well. In genetic forms like X-linked hypophosphatemia, calcium is usually normal but phosphate is markedly low. The pattern of these blood values helps doctors distinguish between calcium-driven and phosphate-driven rickets, which matters because the treatment approach differs.
Treatment for Nutritional Rickets
When rickets is caused by vitamin D deficiency, treatment is straightforward: replace what’s missing. Standard therapy involves daily vitamin D supplementation over about three months. Children aged one to twelve typically receive 3,000 to 6,000 IU per day, while adolescents over twelve receive around 6,000 IU per day. Infants under a year are given a lower dose of about 2,000 IU daily for the same duration.
In some cases, doctors use a single large dose instead. A child between one and twelve years old might receive 150,000 IU as a one-time oral dose, while an adolescent might get 300,000 IU. This approach can be practical when there are concerns about a family’s ability to give daily supplements consistently. Calcium supplements are often added if dietary calcium intake is low.
Most children respond well. Within weeks of starting treatment, blood calcium and phosphate levels begin to normalize, and X-rays show early signs of healing at the growth plates. Mild leg bowing often corrects itself as the bones re-mineralize and the child continues to grow. Severe deformities that persist after medical treatment may eventually require surgical correction.
Genetic Forms Are Harder to Treat
Hereditary rickets like X-linked hypophosphatemia doesn’t resolve with standard vitamin D replacement. These children need phosphate supplements along with specialized forms of vitamin D, and treatment is lifelong rather than a short course. Even with treatment, outcomes for adult height can be disappointing. A study of adults with X-linked hypophosphatemia found no clear evidence that any treatment regimen (high-dose vitamin D, phosphate supplements, or activated vitamin D plus phosphate) improved final adult height. Surgical procedures to straighten bones were sometimes necessary, though having more surgeries was associated with shorter adult stature rather than taller.
Prevention in Infants and Young Children
Preventing nutritional rickets is simple and effective. The CDC recommends that all children under 12 months receive 400 IU of vitamin D daily. Babies who are exclusively breastfed, or who receive a mix of breast milk and formula, should start a vitamin D supplement shortly after birth. Formula-fed babies who drink at least 32 ounces of vitamin D-fortified formula per day generally get enough without an extra supplement.
For older children, regular sun exposure, vitamin D-fortified milk and cereals, and foods naturally rich in vitamin D (fatty fish, egg yolks) help maintain adequate levels. Children with darker skin, those who live at higher latitudes, and those who spend most of their time indoors are at higher risk of deficiency and may benefit from continued supplementation beyond infancy.
Long-Term Outlook
Nutritional rickets caught early and treated promptly has an excellent prognosis. Bones heal, growth resumes, and many skeletal deformities self-correct during childhood. The longer rickets goes untreated, however, the greater the risk of permanent changes: persistent leg bowing, reduced adult height, and dental problems that carry into adulthood. Severe cases may leave lasting curvature in the legs or spine that requires surgical intervention.
For genetic forms, the outlook depends on the specific condition and how early treatment begins. These children benefit from ongoing care with specialists, but some degree of short stature and skeletal irregularity often persists into adulthood despite treatment.