Rickets is a childhood bone disease caused by poor mineralization of the growth plate, the zone of actively growing cartilage near the ends of long bones. The result is bones that are soft, weak, and prone to bending. Although it was largely conquered in wealthy nations by the mid-twentieth century through vitamin D fortification and cod-liver oil, rickets has made an unwelcome comeback in both developing and developed countries, driven by indoor lifestyles, limited sun exposure, and dietary gaps.1PubMed Central. Rickets in Children: An Update Understanding its signs, what causes it, how doctors confirm it, and what treatment looks like can help parents catch it early, when the damage is still fully reversible.
What Rickets Looks Like
Rickets tends to show itself in the parts of the body that are growing fastest. In infants, the skull is a common site: craniotabes (a soft, ping-pong-ball-like give when you press the skull), widened fontanelles, and frontal bossing, where the forehead juts out more than normal.2Journal of Tropical Pediatrics. The Frequency of Nutritional Rickets among Hospitalized Infants and its Relation to Respiratory Diseases Along the ribcage, a row of bead-like bumps at each junction between rib bone and cartilage produces what clinicians call the “rachitic rosary.” A horizontal groove running along the lower chest, known as Harrison’s sulcus, can form where the softened ribs get pulled inward by the diaphragm during breathing.
As children begin to stand and walk, weight-bearing stress bends the weakened leg bones. Bowed legs are the most recognizable sign, but knock-knees can appear instead depending on the child’s age and the pattern of growth. Wrists and ankles look swollen because the growth plates at those joints are widened. Delayed tooth eruption and dental enamel defects are common too, though they are easy to overlook. A study examining rural children in northern China confirmed that five clinical signs are particularly reliable markers of active rickets: wide wrists, frontal bossing, rachitic rosary, Harrison’s sulcus, and bowed legs.3PubMed. Diagnosis of rickets and reassessment of prevalence among rural children in northern China
Beyond the skeleton, children with rickets often have poor muscle tone, which can delay motor milestones like sitting and walking. Irritability, restless sleep, and excessive sweating, particularly around the head, are frequently described by parents. In severe cases, low calcium from the same underlying deficiency can trigger seizures or even heart problems, which brings the disease beyond the bones into genuinely dangerous territory.
The Main Causes
Rickets falls broadly into two categories based on which mineral is in short supply: calcipenic (too little calcium reaching bone) and phosphopenic (too little phosphate). The overwhelming majority of cases worldwide are nutritional, meaning the child does not get enough vitamin D, enough calcium, or both.4PubMed. Nutritional rickets: deficiency of vitamin D, calcium, or both? Vitamin D deficiency and dietary calcium deficiency sit at opposite ends of the spectrum, with many children falling somewhere in between.
Vitamin D is essential because it boosts calcium absorption in the gut. Without it, even a calcium-rich diet cannot deliver enough mineral to the growing skeleton. The body produces vitamin D when ultraviolet B light hits the skin, and it can also come from foods like oily fish, egg yolks, and fortified milk. When a child gets very little sun and eats few fortified foods, vitamin D levels drop and rickets can develop. Even in countries with plenty of sunshine, rickets persists when cultural clothing covers most of the body or when children spend their days indoors.5PubMed Central. Nutritional rickets
Dietary calcium deficiency alone can also cause rickets, even when vitamin D levels are adequate. A landmark trial in Nigerian children showed that those receiving calcium supplements healed substantially better than those receiving vitamin D alone. Roughly 60 percent of children treated with calcium or a combination of calcium and vitamin D reached the study’s healing endpoint, compared with only about 19 percent in the vitamin-D-only group.6PubMed. A comparison of calcium, vitamin D, or both for nutritional rickets in Nigerian children This finding was pivotal because it showed that in populations where diets are low in dairy and calcium-rich foods, fixing vitamin D alone may not be enough.
Genetic and Secondary Forms
A smaller but important group of children develops rickets for reasons that have nothing to do with diet or sunlight. The most common genetic form is X-linked hypophosphatemia (XLH), caused by mutations in the PHEX gene. These mutations lead to overproduction of a hormone called FGF23, which signals the kidneys to dump phosphate into the urine rather than recycling it back into the blood.7PubMed. Hypophosphatemic rickets: lessons from disrupted FGF23 control of phosphorus homeostasis The result is chronically low blood phosphate and bones that cannot mineralize properly.8Nature Reviews Endocrinology. Interdisciplinary management of FGF23-related phosphate wasting syndromes XLH is typically inherited from a parent, though new mutations do occur. Because it is X-linked, both boys and girls can be affected, but the severity can vary.
Other inherited forms exist as well. Vitamin-D-dependent rickets type 1 involves a faulty enzyme that converts vitamin D into its active form, while type 2 involves a defective vitamin D receptor. Both are rare and require specialized treatment beyond simple supplementation.
Chronic kidney disease is another significant secondary cause. The kidneys are where vitamin D gets activated into the hormone that drives calcium absorption. When kidney function deteriorates, this activation step fails, causing poor calcium uptake, rising parathyroid hormone levels, and bone disease that resembles rickets in children who are still growing.9PubMed Central. Chronic kidney disease mineral and bone disorder in children Conditions that impair nutrient absorption in the gut, such as celiac disease, can also lead to rickets because the intestine cannot absorb enough calcium and vitamin D even if the diet supplies them.10PubMed Central. Celiac disease presenting as rickets in Saudi children
Who Is Most at Risk
Certain groups of children are far more vulnerable to nutritional rickets than others. Skin pigmentation plays a large role: melanin acts as a natural sunscreen and reduces the amount of vitamin D the skin produces from the same amount of sunlight. People with darker skin need considerably more sun exposure to synthesize equivalent levels of vitamin D compared to those with lighter skin.11PubMed Central. Colour Counts: Sunlight and Skin Type as Drivers of Vitamin D Deficiency at UK Latitudes At higher latitudes where ultraviolet B is weaker for much of the year, this disparity becomes clinically significant.12PubMed Central. Factors that influence the cutaneous synthesis and dietary sources of vitamin D
Exclusively breastfed infants are another high-risk group. Human breast milk is nutritionally excellent in most respects, but it contains very little vitamin D. Reports from the United States have documented a resurgence of rickets among breastfed infants, particularly dark-skinned infants and those living in northern states, who continue exclusive breastfeeding beyond six months without vitamin D drops.13PubMed. Reemerging nutritional rickets: a historical perspective
Maternal vitamin D status matters too. A severely deficient mother passes inadequate vitamin D stores to her fetus, and some infants are born with overt signs of rickets already present, including craniotabes, wide skull sutures, and low serum calcium.14PubMed. Congenital rickets due to vitamin D deficiency in the mothers Calcium deprivation during pregnancy and early life has been linked to complications ranging from seizures to heart muscle weakness.15PubMed. Complications of vitamin D deficiency from the foetus to the infant: One cause, one prevention, but who’s responsibility?
How Rickets Is Diagnosed
Doctors typically piece together a diagnosis from three angles: clinical examination, blood tests, and X-rays. The clinical signs described earlier, particularly widened wrists, bowed legs, and a rachitic rosary, raise suspicion, but none of them alone is proof. Blood work and imaging confirm the diagnosis and help pinpoint the underlying cause.
Blood Tests
Serum alkaline phosphatase (ALP) is one of the most useful markers. This enzyme rises when bone turnover is abnormally active, and elevated ALP is one of the earliest biochemical signals of rickets in children.16PubMed Central. Alkaline phosphatase in clinical practice in childhood: Focus on rickets ALP levels vary by the type of rickets: children with vitamin-D-dependent rickets tend to have the highest values, while those with hypophosphatemic rickets show more modest elevations. Parathyroid hormone levels follow a similar pattern, running highest in calcipenic forms where the body is desperately trying to pull calcium out of bone.17PubMed Central. Serum Alkaline Phosphatase Levels in Healthy Children and Evaluation of Alkaline Phosphatase z-scores in Different Types of Rickets
Other blood tests include serum calcium, phosphate, and 25-hydroxyvitamin D (the standard measure of vitamin D status). Low calcium with very low vitamin D points to classic nutritional rickets. Low phosphate with normal or near-normal calcium and vitamin D levels points toward a phosphate-wasting condition like XLH. These patterns give clinicians a roadmap for treatment before any genetic testing is needed.
X-ray Findings
X-rays of the wrists and knees are the go-to imaging for suspected rickets. The hallmark findings are widening, cupping, and fraying of the metaphysis, the flared end of the bone just beneath the growth plate.18PubMed Central. Incidental rickets in the emergency department setting These changes occur because unmineralized cartilage accumulates at the growth plate instead of converting smoothly into hard bone. Loss of the bright white line that normally marks the zone of provisional calcification is another reliable sign. A multicenter study of radiologists found that cupping, fraying, and widening of the growth plate were present in rickets but appeared in fewer than 4 percent of children with a different type of bone injury that can mimic rickets on X-rays.19PubMed. Radiologists’ Diagnostic Performance in Differentiation of Rickets and Classic Metaphyseal Lesions on Radiographs: A Multicenter Study
At the growth plate level, what is happening is that phosphate deficiency prevents the normal death of cartilage cells that would ordinarily clear out and be replaced by mineralized bone. Those cartilage cells accumulate, the growth plate expands, and the characteristic radiographic and clinical changes follow, including the swollen-looking wrists and the rachitic rosary along the ribs.20ScienceDirect. Growth plate histology, bone histomorphometry, and radiologic features of nutritional rickets and osteomalacia
Treatment of Nutritional Rickets
When the cause is straightforward vitamin D or calcium deficiency, treatment is gratifyingly effective. High-dose vitamin D, given either as daily oral drops or as a single large intramuscular injection (sometimes called “stoss therapy”), replenishes stores and allows the body to resume absorbing calcium normally. A comparative study in Indian children found that both oral and injectable regimens significantly improved vitamin D levels, calcium, phosphate, ALP, and parathyroid hormone, with radiographic healing confirmed by six months in both groups. The injectable approach produced a more sustained rise in vitamin D and may be easier in settings where daily compliance is a challenge.21PubMed Central. Oral Versus Injectable Vitamin D Therapy for Treating Nutritional Rickets in Indian Children: A Comparative Study
Calcium supplementation alongside vitamin D is standard, especially in populations where dietary calcium intake is low. When rickets is caught early, bone deformities like bowed legs often correct themselves as the child grows and the skeleton re-mineralizes. Surgery is rarely needed for nutritional rickets if treatment starts promptly.
Targeted Treatment for Genetic Forms
Genetic forms of rickets like XLH have historically been harder to manage. The traditional approach involved oral phosphate supplements and active vitamin D, taken multiple times a day for years. Compliance was difficult, the phosphate doses often caused gastrointestinal upset, and the combination sometimes led to kidney calcifications.
A major advance came with burosumab, a monoclonal antibody that blocks the excess FGF23 responsible for phosphate wasting in XLH. In a trial of children with XLH, burosumab injected every two weeks raised serum phosphate into the normal range for more than half of the patients by week six and significantly improved rickets severity scores by week 40.22PubMed. Burosumab Therapy in Children with X-Linked Hypophosphatemia Longer follow-up confirmed the benefits held through at least 160 weeks, with sustained increases in both serum phosphate and phosphate reabsorption by the kidneys, and continued improvement in radiographic rickets scores over that period.23The Journal of Clinical Endocrinology & Metabolism. Sustained Efficacy and Safety of Burosumab, a Monoclonal Antibody to FGF23, in Children With X-Linked Hypophosphatemia Burosumab was approved by multiple regulatory agencies starting in 2018 and has become the treatment of choice for XLH in children.
When Rickets Affects the Heart
Most people think of rickets as a bone disease, and it overwhelmingly is. But the calcium deficiency that underlies many cases does not affect only the skeleton. Calcium is essential for heart muscle contraction, and severe deficiency can weaken the heart. Dilated cardiomyopathy, where the heart chambers stretch and pumping power drops, has been documented in infants with vitamin-D-deficient rickets, sometimes compounded by low magnesium.24PubMed Central. Reversible Dilated Cardiomyopathy Due to Combination of Vitamin D-Deficient Rickets and Primary Hypomagnesemia in an 11-Month-Old Infant The encouraging news is that this form of cardiomyopathy is typically reversible once calcium and vitamin D levels are corrected. Still, it is a reminder that rickets can be more than a cosmetic skeletal problem in its severe forms.
Rickets Versus Osteomalacia
Adults do not get rickets in the classic sense because their growth plates have already fused. The adult equivalent of the same mineralization failure is called osteomalacia, which means “soft bones.” Instead of widened growth plates and bowed legs, osteomalacia shows up as diffuse bone pain, muscle weakness, and a tendency toward fractures. X-rays in osteomalacia may reveal pseudofractures, partial cracks along the surface of the bone, rather than the growth-plate changes seen in children.25Medicine. Rickets and osteomalacia The underlying mechanisms are the same: insufficient vitamin D, calcium, or phosphate prevents bone from hardening properly. Treatment is also similar, though adults obviously do not have the same capacity for skeletal remodeling that growing children do, which means deformities that have already set in are harder to undo.
Prevention
Preventing nutritional rickets is straightforward and inexpensive, which makes its persistence around the world frustrating. Universal vitamin D supplementation starting shortly after birth, regardless of whether the infant is breastfed or formula-fed, is strongly recommended by pediatric guidelines.26PubMed Central. Vitamin D prophylaxis in infancy In most countries, the standard dose is 400 IU per day for the first year of life, with continued supplementation recommended for children at high risk. Formula-fed infants generally get vitamin D through fortified formula, but the amounts can fall short if the baby drinks less than expected.
Adequate maternal vitamin D during pregnancy reduces the risk of congenital and early infantile rickets. For older children, a diet that includes dairy products, fortified cereals, and oily fish helps maintain both vitamin D and calcium intake. Sensible sun exposure, meaning regular brief time outdoors without excessive sunscreen, contributes to vitamin D synthesis. The cod-liver oil that conquered rickets in the early twentieth century worked precisely because it delivered vitamin D in a concentrated, affordable form.27PubMed. Vitamin D, cod-liver oil, sunlight, and rickets: a historical perspective
Surgical Correction of Lingering Deformities
When rickets goes untreated or undertreated for too long, or when a genetic form produces persistent bone abnormalities despite medical therapy, the resulting leg deformities can require surgical correction. The two broad approaches are acute correction (cutting and realigning the bone in one operation, then holding it with hardware) and gradual correction using guided-growth techniques that redirect the growth plate over months.
Timing matters. A study of children with hypophosphatemic rickets who underwent surgical correction of lower-limb deformities found that operating before age 10 carried a significantly higher risk of recurrence. Children younger than 10 at surgery had a roughly fivefold higher hazard of their deformity returning compared to those older than 10. Gradual correction through guided growth also carried a higher recurrence risk than acute osteotomy in this population.28PubMed Central. Predictive factors for recurrence after lower limb deformity correction in hypophosphatemic rickets These findings reflect the reality that in genetic rickets, the underlying metabolic problem keeps pushing the bones out of alignment even after surgery. Waiting until the child is older and the growth plates are less active gives the correction a better chance of lasting. Medical optimization of phosphate levels, now much more achievable with burosumab, is equally important before any surgical intervention.
For nutritional rickets, the picture is more forgiving. Mild to moderate bowing corrects on its own with medical treatment in the majority of young children, and surgery is reserved for severe deformities that persist after biochemical normalization and an adequate observation period.