Rickets is a bone disorder of childhood caused by disrupted mineral metabolism, most often from not getting enough vitamin D, calcium, or both. The disease softens and weakens growing bones, leading to deformities like bowed legs, thickened wrists, and stunted growth. Although it was largely conquered in wealthy nations by the mid-twentieth century through vitamin D fortification of foods, rickets has made a quiet comeback in recent decades, particularly among breastfed infants with limited sun exposure and among populations with darker skin living at higher latitudes.
What Happens Inside Growing Bones
Children’s bones grow at specialized zones near the ends of long bones called growth plates. In healthy development, cartilage cells in these plates multiply, mature, and then die off in an orderly process, making way for new mineralized bone. Rickets disrupts this sequence. When calcium or phosphate levels in the blood drop too low, those cartilage cells fail to die off on schedule, and the growth plate swells with unmineralized tissue instead of being replaced by hard bone.1PubMed Central. Rickets guidance: part I-diagnostic workup The result is bone that bends under the child’s own weight rather than holding its shape. This is why rickets produces visible deformities and why it only occurs while a child is still growing. Adults whose bones have already finished developing can get a related condition called osteomalacia, which softens existing bone rather than warping the growth plate.
The Main Causes
Rickets has more than twenty recognized causes, but the overwhelming majority of cases worldwide fall into two nutritional categories: vitamin D deficiency and calcium deficiency. In temperate and northern climates, vitamin D deficiency is the dominant driver. Breast milk, while ideal in nearly every other nutritional respect, contains very little vitamin D. Infants who are exclusively breastfed without supplementation and who get minimal sun exposure are particularly vulnerable.2PubMed Central. Breastfeeding and vitamin D Indoor lifestyles, sunscreen use, air pollution, and living at high latitudes all reduce the skin’s ability to synthesize vitamin D from sunlight, compounding the problem.
In tropical countries where sunshine is abundant, a different pattern emerges. Children in parts of Nigeria, South Africa, and Bangladesh develop rickets not because they lack vitamin D but because their diets are too low in calcium. Cereal-based diets with little access to dairy products can leave older toddlers and young children chronically calcium-deficient even when their vitamin D levels are adequate.3PubMed. Nutritional rickets: deficiency of vitamin D, calcium, or both? A landmark trial in Nigeria tested vitamin D alone, calcium alone, and the combination in children with rickets. About 61 percent of children given calcium and 58 percent of those given both calcium and vitamin D showed nearly complete healing, compared with only 19 percent of children given vitamin D alone.4PubMed. A comparison of calcium, vitamin D, or both for nutritional rickets in Nigerian children That finding reshaped how clinicians think about rickets in sun-rich regions: when calcium intake is extremely low, adding more vitamin D is not enough.
Who Is Most at Risk
Several overlapping risk factors make certain children far more likely to develop rickets than others. Darker skin produces less vitamin D per hour of sunlight exposure because melanin absorbs the same ultraviolet wavelengths the skin needs for vitamin D synthesis. At the turn of the twentieth century, rickets was nearly universal among African American infants living in northern U.S. cities.5PubMed. Reemerging nutritional rickets: a historical perspective That crisis was solved with vitamin D supplementation and food fortification, but case reports in recent decades show it reemerging among dark-skinned breastfed infants who do not receive vitamin D drops.
Geography matters as well. Children living at higher latitudes, where winter sunlight is too weak to trigger meaningful vitamin D production in the skin, are at greater risk regardless of their complexion. Immigrant families who have moved from equatorial regions to northern Europe or Canada face a compounded disadvantage: darker skin combined with weaker sunlight and, sometimes, cultural practices that limit outdoor exposure. Infants in the polluted industrial cities of early-twentieth-century Europe and the northeastern United States were devastated by rickets for the same reason: smog filtered out the ultraviolet light their skin needed.6PubMed Central. SOLAR ultraviolet radiation and vitamin D: a historical perspective
Exclusive breastfeeding beyond six months without supplementation is another key risk factor. Pediatric guidelines in most countries now recommend that all breastfed infants receive daily vitamin D drops starting in the first days of life, precisely because the breast-milk supply is too low to protect against deficiency on its own.7PubMed Central. Breastfeeding and vitamin D
Recognizing Rickets
The classic signs of rickets are skeletal. Thickened wrists and ankles from widened growth plates, bowing of the legs, a waddling gait, and poor linear growth are the most visible clues. In infants, the soft spot on the skull may remain open longer than expected, the forehead can appear unusually prominent (a feature called frontal bossing), and the skull bones may feel soft and thin when pressed. Bone pain and muscle weakness are common and can make children reluctant to walk or play.
But rickets is not only a bone disease. When blood calcium drops severely, the consequences extend far beyond the skeleton. Young infants with profound vitamin D deficiency can present with seizures, respiratory distress, or even cardiac arrest. A case series of infants aged five to six months documented dangerously low calcium levels alongside severely dilated hearts with ejection fractions as low as 25 to 30 percent, far below the normal range of 55 to 70 percent.8PubMed Central. Cardiac, bone and growth plate manifestations in hypocalcemic infants: revealing the hidden body of the vitamin D deficiency iceberg These infants had developed a form of heart failure driven by calcium deficiency. The encouraging news is that once treated with vitamin D and calcium, cardiac function in these cases returned to normal within months.9PubMed. Hypocalcemic rickets and dilated cardiomyopathy: case reports and review of literature Still, these acute presentations are a stark reminder that rickets can be life-threatening, not merely a skeletal inconvenience.
How Doctors Confirm the Diagnosis
Diagnosis rests on a combination of clinical signs, blood tests, and imaging. X-rays of the wrist or knee are the most informative: they show characteristic fraying and cupping at the ends of the long bones and widening of the growth plates. Blood tests typically reveal elevated alkaline phosphatase, an enzyme whose levels rise when bone turnover is abnormal. Vitamin D, calcium, phosphate, and parathyroid hormone levels help distinguish between different underlying causes. A child with low vitamin D and high parathyroid hormone, for instance, points toward vitamin D deficiency, while normal vitamin D with low calcium and phosphate may suggest dietary calcium deficiency or a genetic form of the disease.
Getting the cause right matters because treatment depends on it. A blanket prescription of vitamin D will not fix calcium-deficiency rickets, and neither vitamin D nor calcium will correct the phosphate-wasting forms caused by genetic mutations. More than twenty acquired or hereditary causes of rickets are now recognized, so the diagnostic workup has to cast a reasonably wide net before settling on a treatment plan.10PubMed Central. Rickets guidance: part I-diagnostic workup
Treating Nutritional Rickets
When the cause is straightforward vitamin D deficiency, treatment involves high-dose vitamin D supplementation for several weeks, followed by a maintenance dose and dietary changes to ensure adequate calcium intake. Most children respond well: X-ray improvement is often visible within weeks, and clinical symptoms like pain and weakness resolve over months. In regions where calcium deficiency is the primary driver, calcium supplementation alone can heal the bone disease, as the Nigerian trial demonstrated.
What catches many parents off guard is that treatment needs to continue well past the point where the child seems better. Bone remodeling is slow, and stopping supplements too early can lead to relapse. Follow-up X-rays and blood tests are used to confirm that healing is genuinely complete before stepping down to a preventive dose.
Genetic Forms and Newer Therapies
Not all rickets is nutritional. Several inherited forms exist, and they do not respond to ordinary vitamin D and calcium supplementation. The most common genetic form is X-linked hypophosphatemia (XLH), caused by mutations in a gene called PHEX on the X chromosome. In XLH, the body wastes phosphate through the kidneys, leaving too little in the blood for proper bone mineralization. Because the gene sits on the X chromosome, XLH can be passed from an affected parent to children of either sex, though boys (who have only one X) tend to be more severely affected. Research into PHEX mutations continues to reveal new variants that reduce the protein’s stability and alter its function, helping explain the range of severity seen across families.11PubMed Central. The PHEX deletion variant (p.Thr605MetfsTer14) causes X-linked hypophosphatemic rickets by reducing protein expression and promoting mineralization
Rarer still are the vitamin D-dependent rickets types I and II (VDDR I and VDDR II). Type I results from a defect in the enzyme that converts vitamin D into its active hormonal form, while type II involves mutations in the receptor that active vitamin D binds to inside cells. Type II is often accompanied by hair loss, sometimes complete, which provides a clinical clue that the problem lies at the receptor level rather than in vitamin D metabolism itself.12PubMed. Vitamin D-dependent rickets type I and type II Type I generally responds to treatment with the active form of vitamin D (calcitriol), whereas type II can be extremely difficult to treat, sometimes requiring very high intravenous calcium infusions to bypass the broken receptor entirely.13Hormone Research. Molecular Genetics of Vitamin D- Dependent Hereditary Rickets
For XLH, a major treatment advance arrived with burosumab, a monoclonal antibody that targets excess FGF23, the hormone driving phosphate wasting. In a clinical trial of children with XLH, burosumab given every two weeks reduced rickets severity scores from an average of 1.9 at baseline to 0.8 by week 40, with improvements persisting at week 64. More than half the children achieved normal blood phosphate levels by week six, and standing-height scores improved over the study period.14PubMed. Burosumab Therapy in Children with X-Linked Hypophosphatemia Real-world observational data have since confirmed these findings, with improvements in pain, quality of life, and biochemical markers during the first six months of treatment.15PubMed Central. Burosumab treatment of X-linked hypophosphatemia patients: interim analysis of the SUNFLOWER longitudinal, observational cohort study Before burosumab, the standard treatment for XLH was frequent oral phosphate and calcitriol, which partially controlled the disease but caused gastrointestinal side effects and required careful monitoring to avoid kidney complications.
Rickets Caused by Other Diseases
Chronic kidney disease is one of the more significant non-nutritional, non-genetic causes of rickets-like bone disease in children. Healthy kidneys perform the final activation step for vitamin D and regulate phosphate excretion. When kidney function declines, both processes go wrong: active vitamin D levels fall, phosphate builds up or is mishandled, and parathyroid hormone climbs in response. Children with long-standing kidney disease commonly develop bony deformities and fractures as a result.16PubMed Central. Bone disease in pediatric chronic kidney disease Managing their bone health requires treating the underlying kidney disorder alongside targeted mineral and hormone supplementation, which is fundamentally different from the approach to nutritional rickets.
Certain medications can also cause rickets-like bone changes. Some anticonvulsant drugs accelerate the liver’s breakdown of vitamin D, and long-term use in children has been linked to bone softening. Conditions that impair fat absorption, such as celiac disease, cystic fibrosis, and inflammatory bowel disease, can interfere with vitamin D uptake from the gut since vitamin D is a fat-soluble vitamin. In all these cases, the treatment must address the underlying condition or its metabolic consequences rather than simply adding more vitamin D.
Prevention and Fortification Policies
The near-elimination of rickets in industrialized countries during the mid-twentieth century is one of public health’s genuine success stories. The key interventions were fortifying milk and infant formula with vitamin D and recommending supplements for breastfed babies. But the policy landscape varies widely even among wealthy nations. Across the Nordic countries, for instance, vitamin D fortification policies range from mandatory and widespread to entirely voluntary, and supplement recommendations differ from covering all age groups to targeting only infants.17PubMed. Vitamin D status and current policies to achieve adequate vitamin D intake in the Nordic countries This patchwork approach means that families who move between countries, or who follow different feeding practices, may fall through the gaps.
For individual families, the prevention message is straightforward. Breastfed infants should receive 400 IU of vitamin D daily starting soon after birth. Formula-fed infants generally get enough from fortified formula, but only if they consume a sufficient volume. Once children transition to solid foods, including dietary sources of vitamin D and calcium (fortified milk, fatty fish, eggs, yogurt) helps maintain adequate levels. Sunlight can contribute, but relying on it alone is unreliable because of the variables involved: latitude, season, skin tone, clothing, sunscreen, and air quality all affect how much vitamin D the skin actually produces.
Long-Term Consequences When Rickets Goes Untreated
Mild rickets caught early and treated properly usually resolves without lasting damage. But severe or prolonged cases can leave permanent skeletal deformities. Bowed legs may persist into adulthood if the disease warps the bones during critical growth periods, sometimes requiring surgical correction. Growth stunting from active rickets can be partly recovered with treatment, but the window narrows as the child ages and growth plates begin to close.
One of the less discussed long-term consequences applies specifically to girls. Severe rickets or osteomalacia during childhood and adolescence can distort the shape of the pelvis. A contracted or flattened pelvis increases the risk of obstructed labor in adulthood, a complication that remains a cause of maternal and infant death in parts of the world where both nutritional deficiency and limited access to obstetric care overlap.18The American Journal of Clinical Nutrition. Nutrition and obstructed labor This connection between childhood nutrition and adult reproductive outcomes illustrates why rickets prevention has consequences that extend well beyond the skeleton and well beyond childhood.
Rickets in Animals
Rickets is not unique to humans. Any growing vertebrate that depends on calcium and phosphate for bone formation can develop it. The condition is well documented in captive mammals, reptiles, and birds, particularly when their diets lack adequate calcium or vitamin D or when they are housed without access to appropriate ultraviolet light. Reptiles kept indoors under standard lighting are especially vulnerable because they rely on UVB radiation to synthesize vitamin D in their skin, just as humans do. The outward signs parallel those in children: bowing of long bones, sometimes severe deformity, and general skeletal weakness.19Crimson Publishers. Metabolic Bone Diseases of Captive Mammal, Reptile and Birds
In veterinary practice, rickets in exotic pets and zoo animals is treated with dietary correction and UV lamp supplementation, much like the nutritional approach in human medicine. The condition is also encountered in farm animals, particularly young livestock raised in confined housing without sunlight. For pet owners, the practical lesson is that species with high calcium or UV requirements, such as iguanas, bearded dragons, and tortoises, need specialized lighting and diet planning rather than the same setup that works for a cat or dog.