Rickets is a childhood bone disorder where growing bones fail to harden properly, leading to soft, weak bones that can bend and deform. It most commonly results from a lack of vitamin D, calcium, or phosphate, and it remains a significant problem worldwide, with rising incidence even in high-income countries.
How Rickets Affects Growing Bones
Children’s long bones grow through a process where cartilage at the ends of bones gradually converts into hard bone tissue. This conversion depends on adequate levels of calcium and phosphate in the blood. When either mineral is too low, the newly formed bone tissue (called osteoid) never fully mineralizes. It stays soft instead of becoming rigid.
The damage concentrates at the growth plates, the strips of cartilage near the ends of long bones where growth happens. Normally, old cartilage cells die off in an orderly way and get replaced by mineralized bone. In rickets, low phosphate levels prevent those cartilage cells from dying on schedule, so they pile up. Blood vessel growth into the area slows down, and the growth plate becomes disorganized and abnormally wide. This widening is visible on X-rays and produces the swollen wrists and ankles that are hallmarks of the disease.
What Causes Rickets
The vast majority of cases trace back to vitamin D deficiency. Your body produces vitamin D when ultraviolet light hits exposed skin, and it also absorbs smaller amounts from food. Children who live in northern climates with limited sunlight, who spend most of their time indoors, or whose skin is heavily covered by clothing are at higher risk. Darker skin pigmentation also reduces vitamin D production. In Saudi Arabia, where sunlight is abundant but cultural dress codes limit skin exposure, studies have found that 100% of young healthy women tested had low vitamin D levels. In India, despite plentiful sun, vitamin D deficiency affects 70% to 100% of the adult population, likely due to widespread vegetarian diets that lack vitamin D-rich foods.
Breastfed infants face a specific risk because human breast milk does not contain enough vitamin D on its own. Children who are lactose intolerant, follow vegetarian diets, or simply don’t consume milk products may also fall short. Not getting enough dietary calcium and phosphorus can cause rickets independently or worsen the effects of low vitamin D.
In developed countries, the prevalence of nutritional rickets is several hundred times higher in dark-skinned immigrant populations compared to native populations, making it an important health equity issue.
Genetic Forms of Rickets
A small number of children develop rickets not from diet or sunlight but from inherited gene mutations. The most common genetic form is X-linked hypophosphatemic rickets, where a mutation causes the kidneys to waste too much phosphate into the urine. No amount of dietary vitamin D will fix this type. Other rare genetic variants involve mutations in the vitamin D receptor itself, making the body unable to respond to vitamin D even when blood levels are normal. These genetic forms require specialized, lifelong treatment with active vitamin D compounds and mineral supplements.
Signs and Symptoms
The physical signs of rickets depend on the child’s age and severity. In infants, early clues include soft skull bones (craniotabes), a prominent forehead, and delayed closure of the soft spot on top of the head. Older infants and toddlers typically show more visible changes: swollen wrists and ankles from widened bone ends, a bumpy pattern along the ribcage where cartilage meets bone (called a rachitic rosary), and failure to thrive.
As children begin to walk and bear weight, leg bowing becomes the most recognizable sign. Legs may curve outward (bowlegs) or inward (knock-knees). Children often develop a waddling gait, bone pain, and muscle weakness. Growth slows noticeably, and affected children tend to be short for their age with disproportionately short legs relative to their trunk.
Severe cases can trigger seizures from dangerously low blood calcium, and dental development suffers too, with delayed tooth eruption and enamel defects.
How Rickets Is Diagnosed
Doctors typically combine a physical exam, blood tests, and X-rays. Blood work checks vitamin D levels, calcium, phosphate, and an enzyme called alkaline phosphatase, which rises when bones are actively breaking down and rebuilding. In children with active rickets, alkaline phosphatase levels are dramatically elevated. A Nigerian study found that children with rickets had average levels of 812 U/L compared to 245 U/L in healthy children. A threshold above 350 U/L identified rickets with 93% sensitivity and 92% specificity in that population.
X-rays of the wrists or knees reveal the characteristic changes: widened, irregular, and frayed-looking growth plates. The ends of the bones appear cupped and splayed rather than smooth and well-defined. These radiographic findings, combined with blood results and clinical signs, confirm the diagnosis and help distinguish nutritional rickets from genetic forms.
Treatment and Recovery
Nutritional rickets responds well to vitamin D and calcium supplementation. Treatment typically involves higher-than-normal doses of vitamin D for about three months, with the dose scaled to the child’s age. Children over age one generally receive 3,000 to 6,000 IU of vitamin D daily during this loading phase, while infants get around 2,000 IU daily. Calcium supplements are given alongside, adjusted for body weight. Some doctors opt for a single large dose instead of daily treatment, which can be practical when daily compliance is uncertain.
After the initial treatment phase, children transition to maintenance doses of 400 to 1,000 IU per day depending on age. X-ray changes typically begin improving within weeks, though complete healing of bone deformities can take months. Mild bowing often corrects itself as the child grows, but severe or longstanding deformities may require bracing or, in rare cases, surgical correction.
Left untreated, rickets leads to permanent bone deformities, failure to grow, dental defects, and recurrent seizures.
Prevention
The simplest prevention strategy is vitamin D supplementation from birth. The CDC, the American Academy of Pediatrics, and the Dietary Guidelines for Americans all recommend that breastfed and partially breastfed infants receive 400 IU of vitamin D daily, starting in the first few days of life. After age one, the recommendation increases to 600 IU daily.
Beyond supplements, regular sun exposure helps, though the amount needed varies with skin tone, latitude, and season. Ensuring adequate dietary calcium through dairy products, fortified foods, or calcium-rich vegetables is equally important. For families following vegetarian or vegan diets, or for children with milk allergies, a daily vitamin D supplement becomes especially critical since their dietary sources are limited.