Rickets is failure of mineralisation of the growth plate and of newly formed osteoid in the growing skeleton, and on radiographs it shows as widening of the physis with loss of the dense zone of provisional calcification, followed by metaphyseal cupping, fraying and splaying. The changes are most obvious where growth is fastest, at the distal femur, proximal tibia, distal radius and ulna and the anterior rib ends, so a single AP wrist and a single AP knee will make the diagnosis in most children. The radiograph tells you that rickets is present and how severe it is; only biochemistry tells you which of the calcipenic or phosphopenic causes is responsible. After the physes fuse the same disease of defective mineralisation is called osteomalacia.
Key facts for practice and radiology board exams
- Earliest change: blurring then loss of the zone of provisional calcification with widening of the lucent physis, before any cupping or fraying is visible.
- Three metaphyseal words: cupping is concavity, fraying is an indistinct brush-like margin, splaying is transverse widening of the metaphysis.
- Films to request: AP wrist plus AP knee. Bilateral films and a full skeletal survey add nothing unless the differential includes abuse, metastases or a dysplasia.
- Alkaline phosphatase is the screening biochemistry: it is raised in essentially all active rickets. A low alkaline phosphatase with rickets-like metaphyses is hypophosphatasia, not rickets.
- Severity and follow-up: the Thacher Rickets Severity Score runs 0 to 10, wrist up to 4 points and knee up to 6, in half point steps [1].
- Nutritional rickets treatment: vitamin D by age band for a minimum of 12 weeks, with at least 500 mg/day of calcium, per the 2016 global consensus [2].
- X-linked hypophosphataemia is now a different disease to manage: burosumab produced substantial radiographic healing in 87 percent of children at week 64 versus 17 percent on conventional phosphate and active vitamin D [3], and is recommended first line for children with overt rickets in the 2025 clinical practice recommendations [4].
- Medicolegal point: vitamin D deficiency without radiographic rickets does not explain fractures in an infant being assessed for non-accidental injury [5].
Quiz
What is the most common cause of rickets?
- Nutritional vitamin D deficiency
- Metabolic bone disease
- Genetic disorder
- Calcium deficiency
Why the metaphysis fails first
Endochondral ossification depends on a calcium and phosphate product high enough to mineralise the cartilage matrix of the hypertrophic zone. When it is not, hypertrophic chondrocytes fail to undergo apoptosis and pile up, the physeal cartilage column lengthens instead of being replaced by bone, and the metaphyseal front is left as soft unmineralised tissue that deforms under load. Low phosphate is the final common pathway in every form of rickets, whether it arrives through vitamin D or calcium deficiency with secondary hyperparathyroidism, or through direct renal phosphate wasting driven by fibroblast growth factor 23 [6][7].
Two consequences matter at the workstation. First, the radiographic changes appear only where a physis is growing quickly, which is why the wrist dominates in infancy and the knee dominates in the toddler and older child. Second, everything you see is a mineralisation problem, so the bone is not just abnormally shaped but abnormally soft, which is why bowing, buckling and Looser zones accompany the metaphyseal signs.
Rickets X-ray findings, sign by sign
| Radiographic sign | What you actually see | Practical note |
|---|---|---|
| Physeal widening | Increase in the lucent gap between epiphysis and metaphysis | Earliest and most sensitive sign; compare with the opposite limb only if uncertain |
| Loss of the zone of provisional calcification | The thin dense white line at the metaphyseal margin blurs then disappears | Its reappearance as a sclerotic band is the first sign of healing |
| Metaphyseal cupping | Concave, cup-shaped metaphyseal margin moulded around the physis | Best seen at the distal ulna, distal femur and proximal tibia |
| Fraying | Indistinct, irregular, brush-like metaphyseal margin, sometimes called a paintbrush metaphysis | Graded together with cupping in the Rickets Severity Score |
| Splaying or flaring | Transverse widening of the metaphysis so that it overhangs the diaphysis | Correlates with the palpable wrist and ankle widening felt clinically |
| Osteopenia with coarse trabeculae | Generalised loss of density with a coarsened, indistinct trabecular pattern | Usually absent in X-linked hypophosphataemia, where density is normal or increased |
| Bowing deformity | Genu varum, genu valgum, coxa vara, anterolateral tibial bowing | Weight bearing accentuates it; varus predominates in the toddler |
| Rachitic rosary | Bulbous expansion of the anterior rib ends at the costochondral junctions | Visible on a chest radiograph obtained for another reason, a common incidental clue |
| Cranial changes | Widened sutures, delayed anterior fontanelle closure, frontal bossing, craniotabes | Frequent in infantile nutritional rickets |
| Looser zones (pseudofractures) | Transverse lucent bands perpendicular to the cortex, often in the medial femoral neck, pubic rami, scapula and ribs | The osteomalacia counterpart, seen in adolescents and adults after physeal fusion |
| Slipped epiphyses and insufficiency fractures | Slipped upper femoral epiphysis, buckling of soft long bones | A soft metaphysis under load, more common in chronic untreated disease |
| Healing periosteal reaction | Smooth subperiosteal new bone plus a dense metaphyseal band | Do not mistake healing rickets for infection or trauma |
Which radiographs to request, by age
| Age | Highest yield site | Why |
|---|---|---|
| Under 1 year, non-ambulant | AP wrist for the distal radius and ulna; anterior rib ends on any chest film | Fastest growing physes at this age; the knee may look near normal early |
| 1 to 3 years | AP wrist and AP knee | Transition period, so image both to avoid a false negative |
| Ambulant child and adolescent | AP knee for the distal femur and proximal tibia, plus standing long leg film if deformity is being measured | Metaphyseal change and mechanical axis deviation are greatest here |
| Any age, monitoring treatment | One AP wrist and one AP knee | These are the two views the Rickets Severity Score is scored on [1] |
A full skeletal survey is not part of the diagnosis of rickets. Request one only when the differential genuinely includes non-accidental injury, metastatic neuroblastoma or a skeletal dysplasia. Cross sectional imaging has no routine role; MRI is reserved for a complication such as a slipped epiphysis or for a suspected tumour causing tumour-induced osteomalacia.
Grading severity: the Thacher Rickets Severity Score
The Rickets Severity Score converts the radiographic appearance into a number so that response to treatment can be compared. It grades the degree of metaphyseal fraying and cupping and the proportion of the growth plate involved on one wrist and one knee radiograph, taking the worse side, and scores the radius and ulna separately at the wrist and the femur and tibia separately at the knee [1].
- Wrist contributes up to 4 points, knee up to 6 points, total 0 to 10 in half point increments, where 0 is a normal radiograph.
- Interobserver correlation was 0.84 or better and intraobserver correlation 0.89 or better in the original series of 67 children with active rickets [1].
- The score correlates only moderately with alkaline phosphatase (r around 0.5), so it complements rather than replaces biochemistry [1][8].
- In X-linked hypophosphataemia, a baseline score of 1.5 or more identified children with worse growth, worse six minute walk distance and more pain, which makes the score prognostic and not merely descriptive [8].
- Trials of healing usually report the score alongside the Radiographic Global Impression of Change, a validated seven point scale from minus 3 to plus 3 that reads paired radiographs side by side [9].
Causes of rickets and their biochemical fingerprints
Rickets is conventionally split into calcipenic forms, driven by deficiency of vitamin D or dietary calcium, and phosphopenic forms, driven by renal phosphate wasting. The radiographs look broadly similar; the laboratory pattern is what separates them.
| Cause | Calcium | Phosphate | ALP | PTH | 25-OH vitamin D | Distinguishing clue |
|---|---|---|---|---|---|---|
| Nutritional vitamin D deficiency | Low or low-normal | Low | High | High | Low | Commonest cause worldwide; dark skin, exclusive breastfeeding without supplementation, limited sun exposure |
| Dietary calcium deficiency | Low or low-normal | Low or normal | High | High | Normal | Low calcium intake diets; 1,25-dihydroxyvitamin D is typically high |
| Vitamin D dependent rickets type 1A (CYP27B1) | Low | Low | High | High | Normal | Low 1,25-dihydroxyvitamin D despite normal 25-OH vitamin D; needs calcitriol, not cholecalciferol |
| Vitamin D dependent rickets type 2A (receptor defect) | Low | Low | High | High | Normal | Markedly high 1,25-dihydroxyvitamin D; alopecia in many patients |
| X-linked hypophosphataemia (PHEX, FGF23 excess) | Normal | Low | High | Normal or mildly high | Normal | Isolated renal phosphate wasting with low tubular reabsorption of phosphate; family history; dental abscesses |
| Chronic kidney disease (renal osteodystrophy) | Low | High | High | Very high | Normal or low | High rather than low phosphate; look for other features of renal bone disease |
| Renal Fanconi syndrome | Normal | Low | High | Normal or high | Normal | Glycosuria, aminoaciduria and proximal renal tubular acidosis accompany the phosphaturia |
| Tumour-induced osteomalacia | Normal | Low | High | Normal | Normal | Adolescent or adult with a small FGF23-secreting mesenchymal tumour; hunt with functional imaging |
| Metabolic bone disease of prematurity | Normal or low | Low | High | Variable | Normal or low | Very low birth weight infant at 6 to 16 weeks; osteopenia and rib fractures dominate |
| Hypophosphatasia (mimic, not rickets) | Normal or high | Normal or high | Low | Normal or low | Normal | Low alkaline phosphatase with lucent metaphyseal tongues; the single most important trap |
Nutritional rickets versus X-linked hypophosphataemia on the radiograph
This is the distinction that changes management, because X-linked hypophosphataemia does not respond to plain vitamin D and now has a targeted treatment. Radiographs give useful pointers even before the biochemistry returns [10].
| Feature | Nutritional rickets | X-linked hypophosphataemia |
|---|---|---|
| Bone density | Generalised osteopenia | Normal or increased, with coarse trabeculae |
| Metaphyseal change | Florid cupping, fraying and splaying, often at every physis imaged | Present but frequently milder than the degree of deformity suggests |
| Deformity | Follows the severity of the metaphyseal disease | Prominent lower limb bowing and coxa vara out of proportion to metaphyseal change |
| Extra-skeletal clues | Rachitic rosary, craniotabes, widened sutures, muscle weakness, hypocalcaemic seizures in infancy | Dental abscesses with normal enamel, enthesopathy in older patients, craniosynostosis, disproportionate short stature |
| Response to cholecalciferol | Heals | Does not heal; needs phosphate with active vitamin D, or burosumab |
Differential diagnosis of the irregular metaphysis
| Entity | How it differs from rickets |
|---|---|
| Newborn stress demineralisation | Metaphyseal lucent bands with an intact zone of provisional calcification, in the first two months of life, resolving spontaneously |
| Classic metaphyseal lesion of infant abuse | Focal corner or bucket-handle fragment with an otherwise sharp, normally mineralised metaphysis and normal alkaline phosphatase |
| Congenital syphilis | Serrated lucent metaphyses, dense metaphyseal bands, diffuse periostitis and focal destruction of the medial proximal tibial metaphysis, the Wimberger corner sign |
| Metastatic neuroblastoma | Metaphyseal lucent bands with permeative destruction, periosteal reaction and sutural splitting; the zone of provisional calcification stays intact |
| Scurvy | Dense zone of provisional calcification rather than a lost one, with the Trummerfeld lucent zone beneath it, the Wimberger ring around epiphyses and subperiosteal haemorrhage |
| Hypophosphatasia | Lucent metaphyseal tongues projecting into the metaphysis with a low serum alkaline phosphatase |
| Metaphyseal chondrodysplasia, Schmid type | Rickets-like metaphyseal irregularity with entirely normal calcium, phosphate, alkaline phosphatase and vitamin D |
| Physiological bowing and Blount disease | Normal physes and metaphyseal mineralisation; Blount shows focal medial proximal tibial beaking and depression |
| Mucopolysaccharidosis | Other features of dysostosis multiplex, including oar-shaped ribs, bullet-shaped metacarpals and inferior vertebral beaking |
Rickets, fractures and suspected child abuse
This question reaches radiologists as an expert opinion request more often than as a diagnostic problem. The evidence is consistent: vitamin D deficiency is common in children, but radiographic rickets is not, and biochemical deficiency alone without radiographic disease has not been shown to cause the fracture patterns seen in abused infants [5]. The 2016 global consensus states that children with radiographically confirmed rickets have an increased fracture risk, while children with simple vitamin D deficiency do not [2]. Report what the radiograph shows, state explicitly whether the metaphyses are rachitic or normally mineralised, and avoid attributing a classic metaphyseal lesion to a low 25-hydroxyvitamin D result in the absence of rachitic change.
Treatment and what healing looks like
The 2016 global consensus on nutritional rickets defines vitamin D sufficiency as a serum 25-hydroxyvitamin D above 50 nmol/L, insufficiency as 30 to 50 nmol/L and deficiency as below 30 nmol/L, and dietary calcium sufficiency in children over 12 months as more than 500 mg/day, insufficiency as 300 to 500 mg/day and deficiency as less than 300 mg/day [2].
| Age | Daily vitamin D for at least 12 weeks | Single high dose alternative | Maintenance after treatment |
|---|---|---|---|
| Under 3 months | 2000 IU/day | Not recommended | 400 IU/day |
| 3 to 12 months | 2000 IU/day | 50,000 IU | 400 IU/day |
| 12 months to 12 years | 3000 to 6000 IU/day | 150,000 IU | 600 IU/day |
| Over 12 years | 6000 IU/day | 300,000 IU | 600 IU/day |
Prevention doses differ from treatment doses: 400 IU/day for all infants in the first year, at least 600 IU/day beyond 12 months, and 600 IU/day in pregnancy [2].
Radiographic healing
- A dense sclerotic line reappears at the metaphyseal margin as the zone of provisional calcification remineralises. This is the earliest radiographic evidence of response.
- The frayed metaphysis fills in and sharpens, physeal width returns towards normal, and periosteal new bone may appear along the shafts.
- Deformity remodels slowly over months to years and is not an early endpoint. Persistent bowing after biochemical cure is a surgical, not a metabolic, question.
- Repeat one wrist and one knee radiograph at around three months, matching the minimum 12 week treatment period, and read it against a falling alkaline phosphatase [2].
- Failure to heal on adequate cholecalciferol should trigger a search for a phosphopenic cause, malabsorption, or poor adherence rather than a higher dose.
X-linked hypophosphataemia
Burosumab, a monoclonal antibody against fibroblast growth factor 23, changed the target in this group. In the randomised phase 3 trial of 61 children aged 1 to 12 years, subcutaneous burosumab 0.8 mg/kg every two weeks gave a Radiographic Global Impression of Change of plus 2.1 at week 64 versus plus 1.0 on conventional oral phosphate with active vitamin D, with substantial healing in 87 percent versus 17 percent, a Rickets Severity Score fall of 2.2 versus 1.0 points and a 33 percent fall in alkaline phosphatase versus 5 percent [3]. The 2025 international clinical practice recommendations now position burosumab as the treatment of choice for children with overt rickets, with radiographs and alkaline phosphatase used to monitor healing [4].
How to report a suspected rachitic radiograph
- State the physes assessed and name them, for example distal radius and ulna, distal femur and proximal tibia.
- Describe the physeal width and whether the zone of provisional calcification is preserved, blurred or lost.
- Describe cupping, fraying and splaying separately, and say which metaphyses are worst affected.
- Comment on bone density and trabecular pattern, since osteopenia points away from X-linked hypophosphataemia.
- Record deformity, including varus or valgus and any Looser zone, insufficiency fracture or slipped epiphysis.
- Give a Rickets Severity Score when the study is a baseline or a follow-up, so that later comparison is objective.
- Explicitly exclude the mimics that alter management: focal corner fractures, permeative metaphyseal destruction, and lucent metaphyseal tongues.
- Close with a recommendation for calcium, phosphate, alkaline phosphatase, parathyroid hormone and 25-hydroxyvitamin D if these are not already available.
Related resources on RadioGyan
- Pediatric bone age calculator, useful when rickets is accompanied by growth failure.
- Normal radiology measurements, for the paediatric reference values quoted in reports.
- Radiology signs index, including the Wimberger and Looser zone signs mentioned above.
Frequently asked questions
References
- Thacher TD, Fischer PR, Pettifor JM, Lawson JO, Manaster BJ, Reading JC. Radiographic scoring method for the assessment of the severity of nutritional rickets. J Trop Pediatr. 2000;46(3):132-139. PMID: 10893912.
- Munns CF, Shaw N, Kiely M, et al. Global consensus recommendations on prevention and management of nutritional rickets. J Clin Endocrinol Metab. 2016;101(2):394-415. PMID: 26745253.
- Imel EA, Glorieux FH, Whyte MP, et al. Burosumab versus conventional therapy in children with X-linked hypophosphataemia: a randomised, active-controlled, open-label, phase 3 trial. Lancet. 2019;393(10189):2416-2427. PMID: 31104833.
- Haffner D, Emma F, Seefried L, et al. Clinical practice recommendations for the diagnosis and management of X-linked hypophosphataemia. Nat Rev Nephrol. 2025;21(5):330-354. PMID: 39814982.
- Aldana Sierra MC, Christian CW. Vitamin D, rickets and child abuse: controversies and evidence. Pediatr Radiol. 2021;51(6):1014-1022. PMID: 33999242.
- Shore RM, Chesney RW. Rickets: part I. Pediatr Radiol. 2013;43(2):140-151. PMID: 23208530.
- Shore RM, Chesney RW. Rickets: part II. Pediatr Radiol. 2013;43(2):152-172. PMID: 23179485.
- Thacher TD, Pettifor JM, Tebben PJ, et al. Rickets severity predicts clinical outcomes in children with X-linked hypophosphatemia: utility of the radiographic Rickets Severity Score. Bone. 2019;122:76-81. PMID: 30772600.
- Lim R, Shailam R, Hulett R, et al. Validation of the Radiographic Global Impression of Change (RGI-C) score to assess healing of rickets in pediatric X-linked hypophosphatemia (XLH). Bone. 2021;148:115964. PMID: 33878504.
- Martel-Villagran J, Arias-Medina A, Garcia-Mardones G. Usefulness of X-rays in the differential diagnosis of hypophosphataemic rickets. Adv Ther. 2020;37(Suppl 2):89-94. PMID: 32236877.
- Chang CY, Rosenthal DI, Mitchell DM, Handa A, Kattapuram SV, Huang AJ. Imaging findings of metabolic bone disease. Radiographics. 2016;36(6):1871-1887. PMID: 27726750.
- Elder CJ, Bishop NJ. Rickets. Lancet. 2014;383(9929):1665-1676. PMID: 24412049.
Case submitted by Dr Vichi Goel MD Radiodiagnosis.
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