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Rickets in Children: Causes, Symptoms, Types & Treatment 

By Dr. Anmol Batra +2 more

Introduction

One of the most common nutritional deficiencies observed in otherwise healthy, growing children is vitamin D deficiency1. A multicentre study across six Indian states involving over 2,500 children (5 to 18 years) found that only 36.8% showed sufficient levels of vitamin D2. Despite India’s abundant sunlight, this deficiency remains highly prevalent and can significantly affect bone health and overall growth.  

Vitamin D, along with calcium and phosphorus, plays a vital role in bone maturation and mineralisation. Thus, inadequate levels of these nutrients could impair proper bone formation, which may lead to conditions like rickets3.

rickets

Through this article, we aim to highlight the importance of addressing vitamin D deficiency and preventing rickets disease in the growing population. 

What is Rickets?

Rickets is a bone disorder that causes the bones of growing children to become soft and weak4.


It occurs when the mineralisation (a process that makes bones strong and rigid) of the growing parts of bones, known as the epiphyseal plates, is defective. In simple terms, this means the bones do not harden properly as they grow.  

Rickets can be inherited (genetic) or acquired (nutritional), with nutritional rickets being the most common form seen worldwide3.

The Role of Vitamin D in Rickets

Vitamin D plays a vital role in maintaining healthy bones by regulating the body’s levels of calcium and phosphorus, the two main minerals responsible for bone strength and structure. It helps the intestines and kidneys absorb calcium and phosphorus from food and urine and ensures that these minerals are properly deposited in growing bones. 

When vitamin D levels are low, the body cannot absorb enough calcium and phosphorus. As a result, bones become soft, weak, and poorly mineralised, leading to rickets in children and osteomalacia in adults. The lack of vitamin D also triggers an increase in parathyroid hormone (PTH), which draws calcium out of bones to maintain normal blood levels, further weakening the skeleton4.

Therefore, ensuring sufficient vitamin D during growth years is crucial to prevent rickets disease, promote bone development, and support overall skeletal health. 

Symptoms of Rickets

Rickets often develops gradually as bones weaken and can affect multiple parts of a child’s body. Common rickets symptoms include3,5:


  • Muscle cramps and general fatigue 
  • Bone pain or tenderness in the arms, legs, pelvis, and spine 
  • Muscle weakness and reduced muscle tone, which may worsen over time 
  • Delayed growth and developmental milestones.  
  • Frequent bone fractures, even after minor injuries 
  • Dental problems, such as delayed tooth eruption, weak enamel, or increased cavities 
  • Excessive irritability is also a feature of vitamin D deficiency. 

Children with rickets disease may also develop skeletal deformities, such as5:

  • Bowed legs or knock knees 
  • An abnormally shaped skull 
  • Bumps along the rib cage (rachitic rosary) 
  • A protruding breastbone (pigeon chest) 
  • Spinal or pelvic deformities 
  • Protruding abdomen 
  • Chronic cough 

Note: Children with rickets are often smaller for their age, and their teeth may appear later than usual6. Thus, early recognition of rickets symptoms is essential to prevent long-term bone deformities and complications. 

Causes of Rickets

The most common cause of rickets is a deficiency of vitamin D, which is essential for calcium and phosphorus absorption and bone mineralisation. In some cases, low calcium or phosphorus intake may also lead to rickets. 

Rickets disease may be nutritional (acquired) or genetic (inherited)3:

  • Nutritional rickets occurs due to inadequate vitamin D from the diet, limited sunlight exposure, or malabsorption (as seen in conditions like celiac disease). 
  • Genetic rickets results from inherited defects that affect vitamin D production, activation, or action in the body. 
  • Certain medications (like anticonvulsants), chronic liver or kidney diseases, and disorders affecting phosphate metabolism may also cause rickets. 

Risk Factors

Rickets most often develops when the body does not get or use enough vitamin D, calcium, or phosphorus, leading to weak and poorly mineralised bones. Children are at a higher risk if they3,5

  • Spend little time outdoors or have limited sun exposure 
  • Have dark skin, which reduces vitamin D synthesis 
  • Are exclusively breastfed without vitamin D supplementation 
  • Live in polluted or high-latitude areas where sunlight exposure is low 
  • Are born preterm or there was maternal deficieny of vitamin D during pregnancy 
  • Suffer from mabsorption syndromes like celiac disease 
  • Primarily have a vegan diet 

Complications of Rickets

If rickets disease is not treated in time, it can lead to3:

  • Poor growth and short height 
  • Weak bones that break easily (multiple fractures) 
  • Bone deformities (such as bowed legs or knock knees) 
  • Abnormal skull growth, which may cause hydrocephalus or increased pressure in the head (ICH) and leads to devlopmental delay. 
  • Dental problems (delayed tooth eruption, weak enamel, dental caries, or underdeveloped teeth) 

If the deficiency becomes severe, low calcium levels can lead to3:

  • Muscle cramps or seizures 
  • Heart and skeletal muscle weakness (myopathy) 

If left untreated, these complications may progress and become life-threatening. 

Diagnosis of Rickets

Diagnosis of rickets is based on clinical evaluation, biochemical investigations, and radiological findings. A detailed medical history and thorough physical examination are essential to identify underlying causes and assess disease severity. 

Laboratory investigations help confirm the diagnosis. Basic tests include3,5:

  • Serum 25-hydroxyvitamin D 
  • Parathyroid hormone (PTH) 
  • Serum alkaline phosphatase (ALP) 
  • Serum/Urine calcium and phosphate 
  • ALP isoenzymes 
  • Blood urea nitrogen (BUN) and creatinine 
  • Liver enzymes 

Radiological evaluation (especially X-rays) is also performed to confirm characteristic bone changes, particularly at rapidly growing sites such as the wrists, knees, and ribs. 

Treatment and Management

Treatment depends on the cause, most commonly a vitamin D or calcium deficiency. The main goals are to correct the deficiency, strengthen bones, and prevent deformities. 

Treatment options include3,7.

  • Vitamin D therapy with daily, weekly, or maintenance regimens 
  • Calcium supplementation to support bone mineralisation 
  • Sunlight exposure to boost natural vitamin D production 
  • Dietary changes to include vitamin D–rich foods  
  • Bracing or corrective surgery for bone deformities (in severe cases) 

Ongoing care3:

  • Regular blood tests for vitamin D, calcium, phosphate, ALP, and PTH 
  • Urine tests to monitor calcium loss 

Note: Genetic forms of rickets are best managed under the care of a paediatric endocrinologist or a metabolic bone specialist. 

Prevention of Rickets

Rickets is caused by vitamin D deficiency and is largely preventable through proper nutrition, sunlight exposure, and supplementation. Key preventive measures include: 

  • Vitamin D and calcium intake: Ensure a diet rich in vitamin D (fortified milk, fish, eggs) and calcium (dairy products, leafy vegetables)3.
  • Sun exposure: Encourage regular, safe sunlight exposure for about 5 to 30 minutes, 2 times a week (more often for darker skin tones) after 6 months of age8.
  • Maternal supplementation: Pregnant women are advised to take vitamin D (under medical guidance) along with other essential nutrients to help prevent deficiency in their babies3.
  • Infant supplementation: Vitamin D drops are recommended for all infants in the first year, and after infancy, for children who are at a higher risk due to poor diet or previous rickets3.
  • Medical care: Kidney or digestive disorders should be treated promptly to improve vitamin D absorption5.
  • Genetic counselling: This is recommended for families with inherited forms of rickets9.

When to Seek Medical Help?

Early medical attention is important to prevent permanent bone damage and complications. Consult a doctor immediately if your child shows3:

  • Delayed growth or walking 
  • Bone pain, tenderness, or deformities (bowed legs, thick wrists/ankles) 
  • Frequent fractures or muscle weakness 
  • Seizures or muscle spasms (possible severe calcium deficiency) 

Conclusion

Rickets is a preventable and treatable condition that primarily results from vitamin D or calcium deficiency.  

Early recognition through clinical evaluation, biochemical tests, and radiological findings is key to effective management. In addition to this, adequate nutrition, sunlight exposure, and timely supplementation during pregnancy and childhood play vital roles in preventing rickets in children. Therefore, parents should keep in mind that with prompt diagnosis and proper treatment, children with rickets can achieve normal growth, strong bones, and healthy development. 

Frequently Asked Questions (FAQs)

Can rickets be corrected?

Yes, rickets can be corrected if detected early. A guided treatment with vitamin D, calcium supplements, and adequate sunlight exposure helps strengthen bones and correct deformities over time3.

Is rickets genetic? 

Most cases are due to vitamin D or calcium deficiency (nutritional rickets), but some rare forms are genetic, caused by inherited problems in vitamin D metabolism or phosphate handling3.

What are anti-rickets?

Anti-rickets refers to nutrients or treatments that prevent or cure rickets10. These are mainly vitamin D, calcium, and phosphorus. They help maintain strong and healthy bones. 

Are bow legs rickets?

Bow legs can be a symptom of rickets, especially in children with soft or weak bones. However, not all bow legs are due to rickets; sometimes, they occur as a normal stage of growth11.

Can you reverse rickets?

In most cases, rickets is reversible with early treatment using vitamin D and calcium. However, long-standing or severe deformities may need braces or surgery for correction3.

References

  1. Suskind DL. Nutritional deficiencies during normal growth. Pediatr Clin North Am. 2009 Oct;56(5):1035-53. Available from:https://pubmed.ncbi.nlm.nih.gov/19931062/ 
  1. Khadilkar A, Kajale N, Oza C, Oke R, Gondhalekar K, Patwardhan V, et al. Vitamin D status and determinants in Indian children and adolescents: a multicentre study. Sci Rep. 2022 Oct 6;12(1):16790. Available from:https://pubmed.ncbi.nlm.nih.gov/36202910/ 
  1. Dahash BA, Sankararaman S. Rickets. Treasure Island [Internet].StatPearls Publishing; [cited 2025 Oct 27]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK562285/ 
  1. Sahay M, Sahay R. Rickets-vitamin D deficiency and dependency. Indian J Endocrinol Metab. 2012 Mar;16(2):164-76. Available from:https://pmc.ncbi.nlm.nih.gov/articles/PMC3313732/ 
  1. MedlinePlus. Rickets [Internet]. National Library of Medicine; [cited 2025 Oct 27]. Available from: https://medlineplus.gov/ency/article/000344.htm 
  1. National Health Service. Rickets and osteomalacia [Internet]. NHS; [cited 2025 Oct 27]. Available from: https://www.nhs.uk/conditions/rickets-and-osteomalacia/ 
  1. Biasucci G, Donini V, Cannalire G. Rickets Types and Treatment with Vitamin D and Analogues. Nutrients. 2024 Jan 31;16(3):416. Available from:https://pmc.ncbi.nlm.nih.gov/articles/PMC10857029/ 
  1. Office of Dietary Supplements (ODS), National Institutes of Health. Vitamin D – Health Professional Fact Sheet [Internet]. NIH; [cited 2025 Oct 27]. Available from: https://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional/ 
  1. Lerch C, Meissner T. Interventions for the prevention of nutritional rickets in term born children. Cochrane Database Syst Rev. 2007 Oct 17;2007(4):CD006164. Available from:https://pmc.ncbi.nlm.nih.gov/articles/PMC8990776/ 
  1. Makishima M. [Rickets/Osteomalacia. The function and mechanism of vitamin D action.]. Clin Calcium. 2018;28(10):1319-1326. Japanese. Available from:https://pubmed.ncbi.nlm.nih.gov/30269113/ 
  1. Vagha K, Jameel PZ, Vagha J, Varma A, Murhekar S, Reddy P, Madirala S. Not all the bowlegs is rickets! (a case report). Pan Afr Med J. 2022 Jun 29;42:161. Available from:https://pmc.ncbi.nlm.nih.gov/articles/PMC9482215/ 

Disclaimer: The information provided here is for educational/awareness purposes only and is not intended to be a substitute for medical treatment by a healthcare professional and should not be relied upon to diagnose or treat any medical condition. The reader should consult a registered medical practitioner to determine the appropriateness of the information and before consuming any medication. PharmEasy does not provide any guarantee or warranty (express or implied) regarding the accuracy, adequacy, completeness, legality, reliability or usefulness of the information; and disclaims any liability arising thereof. 

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