Vitamin D Deficiency: Rickets in Children

Rickets is what a vitamin D deficiency looks like in a growing child. Because a child's bones are still being laid down, a shortage of vitamin D — and the calcium it lets the body absorb — doesn't just thin the skeleton the way it does in adults; it leaves the freshly-built bone soft, so it bends under a toddler's own weight. The classic picture is bowed legs in a child who has just started to stand and walk, along with knobbly wrists and ankles, a delayed crawl or walk, and bones that ache. The reassuring part is that nutritional rickets is almost entirely preventable and treatable: it is caused by something the body lacks, and replacing what's missing usually straightens the bones and lets the child catch up. This page explains what rickets feels like to a child and parent, why low vitamin D specifically softens a child's growing bones, the other things that can mimic it, and how it is diagnosed and corrected.

Table of Contents

1. What Rickets Looks and Feels Like in a Child
2. The Mechanism: Why Low Vitamin D Softens Growing Bone
3. Growth Plates and Bowed Legs
4. Honesty: Not Every Bowed Leg Is Rickets
5. Clues That Point to Vitamin D Rickets
6. Why Children Run Low: Causes and Who Is at Risk
7. Getting Tested and Diagnosed
8. Correcting It: Treatment and Prevention
9. When to Seek Care / Red Flags
10. Key Research Papers
11. Connections
12. Featured Videos

What Rickets Looks and Feels Like in a Child

Rickets rarely announces itself with a single dramatic symptom. More often a parent gradually notices that something about the way their child is growing, moving, or shaped is not quite right. Because the disease affects bone that is actively being built, the signs cluster around the fastest-growing parts of a young skeleton — the legs, the wrists, the ribs, and the skull — and around the milestones that depend on a sturdy frame.

The most recognizable signs include:

• Bowed legs (or knock-knees). The single most famous sign. In a baby just learning to bear weight, the long bones of the lower leg are too soft to hold a straight line and bow outward — the legs curve like parentheses (genu varum). In older toddlers the opposite pattern, knock-knees (genu valgum), can appear instead. The bowing typically becomes obvious once the child starts pulling to stand and walking, because that is when weight first loads the soft bone.
• Knobbly wrists and ankles. The ends of the long bones, where growth happens, widen and feel lumpy. Parents and clinicians can often feel a bony swelling at the wrist.
• The “rachitic rosary.” A row of bead-like bumps along the front of the ribcage, where each rib meets its cartilage, caused by the same widening of growing bone.
• A soft or oddly-shaped skull. In infants the skull bones can feel soft (a sign called craniotabes), the soft spot (fontanelle) may close late, and the forehead can look prominent or “bossed.”
• Delayed milestones and reluctance to move. Late sitting, crawling, standing, or walking; a child who would rather be carried; or one who seems to find weight-bearing uncomfortable.
• Bone pain and tenderness. Many children with rickets are simply achy — fussy, unwilling to walk far, sore to handle — without being able to say where it hurts.
• Slow growth and short stature. Over months, growth in length can stall, so the child drifts downward on the growth chart.
• Dental problems. Teeth may come in late, and the enamel can be poorly formed and prone to cavities.

Two more serious presentations are worth naming because they can be the first sign of rickets and are medical emergencies. Severe deficiency can drop the blood calcium low enough to cause seizures or muscle twitching (tetany), sometimes in a baby who looks otherwise well, and the weak chest wall and floppy muscles of advanced rickets can contribute to breathing problems and chest infections in infants. These are covered under Red Flags.

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The Mechanism: Why Low Vitamin D Softens Growing Bone

To understand rickets, it helps to know the one job vitamin D does that matters most here: it is the body's calcium-absorption switch. Vitamin D (made in skin from sunlight, or taken in from food and supplements) is converted by the liver and then the kidney into its active hormone form, calcitriol. Calcitriol acts on the lining of the gut to switch on the machinery that pulls calcium — and, to a lesser degree, phosphorus — out of food and into the blood. Without enough vitamin D, a child can eat a perfectly reasonable amount of calcium and still absorb only a fraction of it.

Bone is built from a protein scaffold (collagen) that then gets hardened by crystals of calcium and phosphate — a process called mineralization. Think of bone like reinforced concrete: the collagen is the steel rebar, and the calcium-phosphate mineral is the concrete poured around it that makes the structure rigid and able to bear weight. When vitamin D is low, blood calcium tends to fall; the body responds by releasing more parathyroid hormone (PTH), which props the blood calcium back up partly by pulling phosphorus out through the kidneys. The result is that the building site runs short of the very minerals it needs — especially phosphate — so the freshly-laid collagen scaffold never gets properly hardened. The rebar goes up, but the concrete is watered down. The bone that forms is soft, unmineralized, and weak.

In an adult, whose skeleton has stopped growing, the same defect produces osteomalacia — soft, painful bone. Rickets is the childhood version of the very same disease, but with an extra dimension: it strikes bone that is still being created and lengthened. That is why rickets deforms the skeleton in ways adult deficiency cannot, and why its signs concentrate at the growth plates.

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Growth Plates and Bowed Legs

The reason rickets and adult bone disease look so different comes down to the growth plate (the physis) — a band of living cartilage near the ends of a child's long bones where new bone is manufactured to make the child taller. A growth plate works like an assembly line: cartilage cells line up in orderly columns, multiply, swell, and then are mineralized and converted into solid bone, lengthening the limb a little at a time.

That assembly line depends utterly on a steady supply of calcium and phosphate. When vitamin D deficiency starves it of minerals, the line jams. The cartilage cells keep being produced but fail to mineralize and mature on schedule, so the growth plate piles up, disorganizes, and widens. This is exactly what produces the visible knobbly wrists and ankles and the rachitic rosary at the ribs — you are seeing swollen, mineral-starved growth plates through the skin. On an X-ray the same change shows up as growth plates that look widened, frayed, and cupped, which is one of the most reliable signs radiologists look for.

The bowing of the legs follows from simple mechanics. Around the end of the first year, a baby starts pulling to stand and taking first steps — loading the long bones of the lower leg with body weight for the first time. In a healthy child those bones are rigid enough to take it. In a child with rickets they are soft, so they bend under the load, the way a green twig bows where a dry stick would snap. Standing and walking concentrate the force, which is why bowed legs so often appear right around the time a child becomes mobile, and why the deformity tends to worsen the more the child walks until the underlying deficiency is treated. The encouraging flip side is that because this same bone is still actively remodeling, correcting the deficiency early often lets the legs straighten on their own as the child keeps growing.

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Honesty: Not Every Bowed Leg Is Rickets

It is important to say plainly: most bowed legs in babies are completely normal, and most children with bowed legs do not have rickets. A degree of bowing is a normal stage of development, and several other conditions can cause leg deformity. Jumping to “rickets” the moment a toddler looks bow-legged would frighten a great many parents needlessly. The honest picture:

• Physiologic (normal) bowing. Nearly all infants are somewhat bow-legged — a holdover from their folded position in the womb. It is symmetric, painless, and resolves on its own, usually straightening out by around age two or three (often passing through a knock-kneed phase before settling). This is by far the most common reason a baby looks bow-legged, and it needs no treatment.
• Blount disease. A growth disorder of the shin bone (tibia) that causes progressive, often one-sided bowing. It is not caused by vitamin D and does not respond to it; it is diagnosed by its X-ray appearance and managed orthopedically.
• Genetic and inherited forms of rickets. Some rickets is not nutritional at all. X-linked hypophosphatemic rickets and other inherited disorders cause the kidneys to waste phosphate; these children bow their legs from a phosphate problem, not a lack of vitamin D, and they need entirely different, specialist treatment. Rare inherited defects in activating or responding to vitamin D exist as well.
• Other skeletal and metabolic conditions. Skeletal dysplasias (such as achondroplasia), old fractures or injury to a growth plate, and chronic kidney disease can each deform growing bone.

The takeaway is not to panic over a chubby, symmetric, painless bow in a thriving one-year-old — but also not to dismiss bowing that is worsening, one-sided, painful, or paired with the other signs below. Telling these apart is exactly what a clinical exam, a blood test, and (when needed) an X-ray are for.

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Clues That Point to Vitamin D Rickets

Certain features make nutritional vitamin D rickets — as opposed to normal bowing or another cause — much more likely. None is proof on its own, but together they form a recognizable pattern:

• The bowing is paired with bone changes elsewhere — widened, knobbly wrists and ankles, a rachitic rosary on the ribs, or a soft skull — rather than being the only finding. Rickets is a whole-skeleton disease; isolated leg bowing with everything else normal points away from it.
• It worsens rather than improves with age. Normal physiologic bowing gets better after the toddler years. Bowing that deepens, especially after age two, is a warning sign.
• There are matching risk factors. A breastfed infant not given a vitamin D supplement, darker skin, little sun exposure or fully-covered clothing, a northern latitude or winter, a restrictive or dairy-free diet, or known malabsorption all raise the odds (see the next section).
• Growth and milestones are off. Slowing growth, late walking, and reluctance to bear weight alongside the bone changes strengthen the case.
• There may be hints of low calcium. Muscle cramps, twitching, irritability, or — at the severe end — a seizure can accompany the skeletal signs.

Several of these symptoms overlap with siblings in this deficiency family. A child or older teen may also show the muscle weakness that vitamin D deficiency causes, and the diffuse aching of soft bone is the pediatric face of the same bone pain and osteomalacia seen in adults. What sets rickets apart is the deformity of growing bone — the bowed legs and widened growth plates — which only happens while the skeleton is still being built.

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Why Children Run Low: Causes and Who Is at Risk

Nutritional rickets comes from too little vitamin D, too little calcium, or both. Understanding the common routes makes it clear why certain children are far more vulnerable — and why most cases are preventable.

• Exclusive breastfeeding without a supplement. Breast milk is superb in almost every respect but is naturally low in vitamin D. A baby who is breastfed and not given a vitamin D supplement is the single most common setting for nutritional rickets in well-resourced countries. This is precisely why pediatric guidelines recommend a daily vitamin D supplement for breastfed infants from the first days of life.
• Darker skin. Melanin is a natural sunscreen; more pigment means a child needs considerably more sun exposure to make the same vitamin D. Children with darker skin are over-represented in rickets cases, especially at higher latitudes.
• Little sun exposure. Living far from the equator, long winters, staying indoors, covering the skin for cultural or sun-protection reasons, and air pollution all cut the skin's vitamin D production. Sunscreen, used as recommended for skin-cancer prevention, also reduces it — which is part of why dietary and supplemental vitamin D matter.
• Low dietary calcium. In many parts of the world, rickets is driven as much by a calcium-poor diet as by vitamin D shortage — for example diets very low in dairy and other calcium sources. A child can have adequate vitamin D and still develop rickets if calcium intake is very low.
• Restrictive or unfortified diets. Dairy-free, vegan, or otherwise limited diets without deliberate fortification or supplementation; some restrictive feeding practices; and a few cases tied to unbalanced milk-substitute use.
• Malabsorption and medical conditions. Vitamin D is fat-soluble, so anything that impairs fat absorption lowers it: celiac disease, Crohn's disease and other inflammatory bowel disease, cystic fibrosis, and cholestatic liver disease. Chronic kidney disease impairs the final activation step. Certain medicines (some anti-seizure drugs and glucocorticoids) speed vitamin D breakdown.
• Prematurity and rapid growth. Premature babies are born with low stores and a fast-growing skeleton, putting heavy demand on calcium, phosphorus, and vitamin D.

A child who is breastfed without a supplement, has darker skin, and gets little sun in a northern winter carries several of these at once — which is exactly the combination behind the resurgence of nutritional rickets reported in recent decades, even in wealthy countries where the disease had been thought conquered.

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Getting Tested and Diagnosed

Diagnosing rickets is usually straightforward and combines a clinical exam, a blood test, and an X-ray. None is expensive, and together they both confirm the diagnosis and reveal the cause.

Blood tests. The cornerstone is the 25-hydroxyvitamin D test, which measures the body's vitamin D stores and is typically low. But rickets is a biochemical pattern, not a single number, and a panel is what clinches it. A classic rickets profile shows a high alkaline phosphatase (an enzyme that pours out of busy, struggling bone — one of the most useful clues in children), often a low or low-normal calcium, a low phosphate, and a raised parathyroid hormone (PTH) as the body fights to keep blood calcium up. Measuring phosphate and PTH also helps separate ordinary nutritional rickets from the inherited phosphate-wasting forms, which need different treatment.

X-rays. A plain X-ray of the wrist or knee is the classic confirmation. The growth plates look widened, frayed (“paintbrush”), and cupped, the ends of the bones are poorly mineralized, and the overall bone looks washed-out. These changes are characteristic enough that an X-ray often settles the diagnosis and provides a baseline to track healing — on follow-up films, a sharp line of new mineral appearing at the growth plate is the welcome sign that treatment is working.

Because so many things can bow a child's legs, this workup is what distinguishes nutritional vitamin D rickets from normal bowing, Blount disease, and the genetic forms — and it is why a clinician will usually want bloods and an image rather than treating on appearance alone.

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Correcting It: Treatment and Prevention

The hopeful heart of this page: nutritional rickets is highly treatable, and caught early it usually heals with the bones straightening as the child grows. Treatment has two parts — replacing what's missing, and keeping it from coming back — and it should be guided by a clinician, because the doses for a deficient child are specific and depend on age.

• Replacing vitamin D. Treatment uses a defined course of vitamin D (cholecalciferol, D3, or sometimes ergocalciferol, D2) at therapeutic doses far higher than the small daily preventive dose, given either as a daily amount over several weeks or, in some protocols, as a single large supervised dose — followed by ongoing maintenance. The exact regimen is matched to the child's age and the local guideline, which is why this is prescribed and monitored rather than self-dosed.
• Don't forget the calcium. A crucial, often-overlooked point from the research: vitamin D alone may not fully heal rickets if the child's calcium intake is low. International guidelines recommend giving adequate calcium alongside the vitamin D — from diet where possible, with a supplement if needed — because in many children the bone simply lacks the raw material to remineralize. Where the rickets is driven mainly by dietary calcium shortage, calcium is the key part of the cure.
• Food and sensible sunlight afterward. Once treated, prevention leans on vitamin D–rich and fortified foods — cod liver oil (the historic rickets remedy), oily fish such as salmon and sardines, egg yolks, and fortified milk — plus calcium-rich foods, and reasonable (not burning) sun exposure where appropriate.
• Ongoing supplementation for those at risk. Continued daily vitamin D is recommended for breastfed infants and other at-risk children to keep the deficiency from returning.
• Treat any underlying cause. If malabsorption (such as celiac disease), kidney disease, or a medication is behind the deficiency, that has to be addressed too — and the inherited, phosphate-wasting forms of rickets need entirely different, specialist treatment, which is why getting the diagnosis right first matters.

Prevention is the real win. The reason rickets became rare in the twentieth century is that countries began fortifying foods and supplementing infants. Giving a breastfed baby a daily vitamin D supplement from birth, and making sure children get enough calcium and vitamin D as they grow, prevents the overwhelming majority of nutritional rickets before it can ever start. For the broader picture of vitamin D's role in the skeleton across life, see Vitamin D3 and Bone Health and the Vitamin D3 Benefits hub.

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When to Seek Care / Red Flags

Most signs of rickets call for a calm, prompt appointment with a pediatrician rather than an emergency — but a few features mean a child should be seen urgently or by emergency services, because severe vitamin D deficiency can drop the blood calcium dangerously low:

• A seizure or convulsion in an infant or child — especially in a baby not previously known to have epilepsy — can be the first sign of dangerously low calcium from rickets. This is an emergency.
• Twitching, jerking, muscle spasms, or stiffening (tetany), or unusual irritability and jitteriness in a baby.
• Difficulty breathing or repeated chest infections in an infant, which the soft chest wall and weak muscles of severe rickets can contribute to.
• Poor feeding, lethargy, or a baby who is “not themselves” alongside any of the bone signs.

Short of those emergencies, see a clinician promptly — not as an emergency, but without long delay — for bowed legs that are worsening, one-sided, or painful, for knobbly wrists or a rachitic rosary, for a child who is slow to walk or reluctant to bear weight, or for stalling growth. Nutritional rickets responds well to treatment, but the earlier it is caught, the more completely the bones straighten and the lower the risk of any lasting deformity. When in doubt about a child's bones or growth, a quick exam and a single blood test can settle it.

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Key Research Papers

1. Holick MF (2007). Vitamin D Deficiency. New England Journal of Medicine;357(3):266-281. — DOI: 10.1056/NEJMra070553
2. Munns CF, Shaw N, Kiely M, et al. (2016). Global Consensus Recommendations on Prevention and Management of Nutritional Rickets. Journal of Clinical Endocrinology & Metabolism;101(2):394-415. — DOI: 10.1210/jc.2015-2175
3. Misra M, Pacaud D, Petryk A, et al. (2008). Vitamin D Deficiency in Children and Its Management: Review of Current Knowledge and Recommendations. Pediatrics;122(2):398-417. — DOI: 10.1542/peds.2008-1862
4. Weisberg P, Scanlon KS, Li R, Cogswell ME (2004). Nutritional rickets among children in the United States: review of cases reported between 1986 and 2003. American Journal of Clinical Nutrition;80(6):1697S-1705S. — DOI: 10.1093/ajcn/80.6.1697S
5. Pettifor JM (2004). Nutritional rickets: deficiency of vitamin D, calcium, or both? American Journal of Clinical Nutrition;80(6):1725S-1729S. — DOI: 10.1093/ajcn/80.6.1725S
6. Holick MF (2006). Resurrection of vitamin D deficiency and rickets. Journal of Clinical Investigation;116(8):2062-2072. — DOI: 10.1172/JCI29449
7. Elder CJ, Bishop NJ (2014). Rickets. The Lancet;383(9929):1665-1676. — DOI: 10.1016/S0140-6736(13)61650-5
8. Carpenter TO, Shaw NJ, Portale AA, et al. (2017). Rickets. Nature Reviews Disease Primers;3:17101. — DOI: 10.1038/nrdp.2017.101
9. Rajakumar K (2003). Vitamin D, Cod-Liver Oil, Sunlight, and Rickets: A Historical Perspective. Pediatrics;112(2):e132-e135. — DOI: 10.1542/peds.112.2.e132
10. Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. (2011). Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an Endocrine Society Clinical Practice Guideline. Journal of Clinical Endocrinology & Metabolism;96(7):1911-1930. — DOI: 10.1210/jc.2011-0385
11. Wharton B, Bishop N (2003). Rickets. The Lancet;362(9393):1389-1400. — PubMed
12. Thacher TD, Fischer PR, Strand MA, Pettifor JM (2006). Nutritional rickets around the world: causes and future directions. Annals of Tropical Paediatrics;26(1):1-16. — PubMed

PubMed Topic Searches

• PubMed — Nutritional rickets in children and vitamin D
• PubMed — Rickets, bowed legs, and genu varum in children
• PubMed — Vitamin D deficiency in breastfed infants and rickets
• PubMed — Hypocalcemic seizures and rickets in infants
• PubMed — Rickets, calcium intake, and treatment in children

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Connections

• Vitamin D Deficiency Hub
• Bone Pain & Osteomalacia
• Muscle Weakness & Falls
• Fatigue & Low Mood
• Vitamin D3 Overview
• Vitamin D3 Benefits
• Vitamin D3 and Bone Health
• Vitamin D Test (25-Hydroxyvitamin D)
• Calcium
• Phosphorus
• Celiac Disease
• Crohn's Disease
• Kidney Disease
• Cod Liver Oil
• Salmon
• Eggs

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