What is Rickets?

Rickets occurs when growing bones and growth plates do not receive or use enough calcium and phosphate for normal mineralisation. Growth plates are areas of developing tissue near the ends of long bones where new bone forms as a child grows.

Vitamin D helps the body absorb and regulate calcium and phosphate. When the availability or metabolism of these minerals is disrupted, growth plates may widen and growing bones can become softer and weaker.

Rickets occurs while the skeleton is still growing and the growth plates remain open. After skeletal growth is complete, a similar mineralisation disorder affecting mature bone is called osteomalacia.

What are the Types of Rickets?

Rickets can be broadly classified according to the mineral imbalance responsible for abnormal bone mineralisation. These types of rickets are mentioned below:

  1. Calciopenic Rickets Calciopenic rickets occurs when there is not enough calcium available for normal bone mineralisation. Important forms include:
    • Nutritional Rickets: Usually caused by vitamin D deficiency, inadequate calcium intake or both.
    • Vitamin D-Dependent Rickets: Rare inherited disorders in which the body cannot properly activate vitamin D or respond to its active form.
    • Rickets Related to Malabsorption or Liver Disease: Conditions affecting the absorption or metabolism of vitamin D and calcium may lead to rickets.
  2. Phosphopenic Rickets Phosphopenic rickets occurs when phosphate levels remain too low for normal bone development. It can occur in three forms:
    • Inherited Hypophosphataemic Rickets: Genetic disorders such as X-linked hypophosphataemia cause excessive phosphate loss through the kidneys.
    • Renal Tubular Disorders: Certain kidney disorders cause excessive phosphate loss in urine.
    • Acquired Phosphate-Wasting Rickets: Less commonly, other medical conditions can lead to persistent phosphate loss.
  3. Kidney-Related Rickets Chronic kidney disease can disturb calcium, phosphate and active vitamin D regulation, leading to abnormal bone mineralisation and rickets-like skeletal changes in growing children. Knowing the exact type of rickets is important, as treatment differs considerably between nutritional, inherited, phosphate-wasting and kidney-related forms.

How Common is Rickets in India?

Rickets is a prevalent childhood bone disorder in India, particularly among younger children. As per a clinical study in 2020, 46% of children aged under 10 years are at risk of developing rickets. However, a national survey to provide the exact number of rickets cases in India is unavailable.

What are the Stages of Rickets?

Rickets does not have a universal staging system that applies to every type of the condition. Three biochemical stages have been described for vitamin D-deficiency rickets, but these should not be applied to inherited, kidney-related or phosphate-wasting forms.

The table below shows the typical features of vitamin D deficiency rickets based on its stages:

Stage Typical Features
Stage 1 Vitamin D levels fall. Calcium may remain normal or begin to decrease, while phosphate is often still normal. PTH and alkaline phosphatase may begin to rise.
Stage 2 Phosphate levels decrease and PTH and alkaline phosphatase become more clearly elevated as the body tries to maintain blood calcium levels.
Stage 3 Calcium and phosphate may become markedly low, while PTH and alkaline phosphatase rise substantially. Skeletal and clinical features are usually more established.

What are the Symptoms of Rickets?

The signs of rickets vary according to the child's age, severity and stage of skeletal development. Infants may first develop skull or muscle changes, while leg deformities become more noticeable after a child begins standing and walking.

The early warning signs and advanced stage symptoms of rickets are listed in the table below:

Early Warning Signs Advanced Stage Symptoms
  • Soft skull bones

  • Large or slow-closing fontanelle

  • Frontal bossing

  • Muscle weakness

  • Delayed sitting, standing or walking

  • Poor growth

  • Delayed tooth eruption

  • Widened wrists or ankles

  • Bowed legs

  • Knock knees

  • Rachitic rosary

  • Waddling gait

  • More obvious skeletal deformities

  • Bone pain or fractures

Craniotabes refers to unusual softness of the skull bones and may appear in infants. A large or slow-closing fontanelle can also occur.

As children grow and begin bearing weight, the ends of long bones may widen, causing noticeable enlargement around the wrists and ankles. Bowed legs or knock knees may then become more apparent.

A rachitic rosary refers to bead-like enlargements where the ribs meet their cartilage along the front of the chest.

Diseases Similar to Rickets

Several childhood skeletal disorders like Blount disease or hypophosphatasia can resemble rickets, as they may cause bowed legs, bone deformity, abnormal growth or difficulty walking.

A comparative overview of these three conditions is given below, highlighting their distinct features:

Rickets Vs. Blount Disease Vs. Hypophosphatasia

Feature Rickets Blount Disease Hypophosphatasia
How It Happens Poor mineralisation of growing bone due to calcium, phosphate, vitamin D or metabolic abnormalities Abnormal growth of the upper part of the tibia causes progressive bowing An inherited enzyme deficiency interferes with normal bone and tooth mineralisation
Location Growth plates throughout the growing skeleton Mainly the upper tibia and lower limbs Bones and teeth; distribution varies with severity
Associated Symptoms Widened wrists, bowed legs, growth delay, muscle weakness and skeletal deformity Progressive bowing of the legs, often without typical wrist or rib changes of rickets Poor mineralisation, bone deformity, fractures and premature loss of teeth
Severity Varies from mild nutritional disease to severe inherited forms Can progress and cause significant leg deformity Ranges from mild dental disease to severe skeletal disease
Can It Be Reversed? Nutritional forms often improve substantially when the underlying deficiency is corrected Treatment depends on age and severity and may include bracing or surgery Requires condition-specific management; severity and long-term outlook vary

Blood tests and X-rays help distinguish rickets from conditions that produce similar skeletal changes.

What Causes Rickets?

Rickets develops when growing bones do not have enough available calcium or phosphate to mineralise properly. The possible causes of rickets are given below:

  • Vitamin D Deficiency: Inadequate vitamin D reduces calcium absorption from the intestine and can lead to nutritional rickets.

  • Low Calcium Intake: A diet that provides too little calcium can impair bone mineralisation even when vitamin D levels are not severely reduced.

  • Phosphate Loss: Certain kidney disorders cause excessive phosphate loss in urine, leaving too little available for growing bones.

  • Inherited Vitamin D Disorders: Rare genetic conditions can interfere with vitamin D activation or prevent the body from responding normally to active vitamin D.

  • Kidney Disorders: Chronic kidney disease and renal tubular disorders can disturb calcium, phosphate and vitamin D regulation.

  • Malabsorption: Intestinal conditions that interfere with nutrient absorption can reduce the availability of vitamin D and calcium.

  • Liver Disease: Significant liver disease can interfere with vitamin D metabolism and contribute to abnormal mineral balance.

What are the Risk Factors for Rickets?

Risk factors depend on the underlying type of rickets. These factors are listed below:

  • Inadequate Vitamin D: Low vitamin D intake or inadequate supplementation can increase the risk of deficiency-related rickets.

  • Low Calcium Intake: A diet consistently low in calcium can interfere with normal bone mineralisation.

  • Limited Sunlight Exposure: Very limited ultraviolet exposure can reduce vitamin D production in the skin.

  • Darker Skin Pigmentation: Higher melanin levels can reduce vitamin D production from sunlight.

  • Rapid Growth: Infants, children and adolescents have greater mineral requirements during periods of rapid skeletal growth.

  • Malabsorption Disorders: Conditions that reduce absorption of vitamin D or calcium can increase the risk of rickets.

  • Kidney Disease: Kidney disorders may interfere with phosphate balance and activation of vitamin D.

  • Liver Disease: Chronic liver disease can affect vitamin D metabolism.

  • Family History or Genetic Disorders: Inherited abnormalities involving vitamin D or phosphate metabolism are known to cause certain forms of rickets.

  • Certain Medicines: Long-term use of some medicines may interfere with vitamin D or bone metabolism.

What are the Complications of Rickets?

Untreated or severe rickets can affect skeletal growth, bone strength and development. Complications associated with rickets are mentioned below:

  • Persistent Skeletal Deformities: Bowed legs, knock knees and other limb deformities can become more pronounced as a child grows.

  • Growth Impairment: Long-standing disease can slow normal skeletal growth and contribute to short stature.

  • Bone Fractures: Poorly mineralised bones are weaker and may fracture more easily.

  • Delayed Motor Development: Muscle weakness and skeletal changes can delay sitting, standing or walking.

  • Dental Problems: Delayed tooth eruption and enamel abnormalities may occur in some forms of rickets.

  • Severe Hypocalcaemia: Very low calcium levels can lead to muscle spasms, tetany or seizures and require urgent treatment.

When Should I See a Healthcare Provider?

Seeking medical assessment is recommended if a child develops:

  • Bowed legs or knock knees that appear excessive or worsen

  • Widening of the wrists or ankles

  • Delayed growth

  • Delayed sitting, standing or walking

  • Persistent muscle weakness

  • Bone pain

  • Frequent or unexplained fractures

  • Delayed tooth eruption

  • Skull or chest-wall changes suggestive of rickets

Urgent medical attention is required if a child develops seizures, severe muscle spasms, difficulty breathing or other symptoms that could indicate severely low calcium levels.

How is Rickets Diagnosed?

Rickets is diagnosed using a combination of medical history, physical examination, blood tests and X-rays.

The following tests and assessments may be conducted by doctors to diagnose rickets:

  1. Clinical Examination The doctor may examine the child's growth, limb alignment, wrists, ankles, chest and skull. Walking pattern, muscle strength and motor development may also be assessed. The medical history may include information about diet, calcium intake, vitamin D supplementation, previous illnesses, medicines, family history and symptoms suggesting kidney, liver or intestinal disease.

  2. Blood Tests Blood tests help identify the mineral imbalance and determine the likely cause of rickets. Common tests include calcium, phosphate, alkaline phosphatase, parathyroid hormone and 25-hydroxyvitamin D. Kidney function, electrolytes and additional investigations may be checked when an inherited, renal or metabolic cause is suspected. Alkaline phosphatase is typically elevated in active rickets. A persistently low level may suggest hypophosphatasia.

  3. X-Rays

    X-rays can confirm characteristic changes at rapidly growing ends of bones, particularly around the wrists, knees and ankles.

    Typical findings include:

    • Cupping: The end of a growing bone develops a concave appearance.
    • Fraying: The edge of the growing bone becomes irregular.
    • Splaying: The bone end becomes wider than normal.
    • Growth-Plate Widening: The space around the growth plate becomes enlarged.

Diagnostic Summary Table

Test What It Assesses
Serum calcium Calcium balance
Serum phosphate Phosphate availability
Alkaline phosphatase Bone mineralisation activity
25-OH vitamin D Vitamin D status
PTH Response to calcium and vitamin D imbalance
Kidney function tests Possible renal contribution
X-ray Characteristic growth-plate abnormalities

Children whose results do not fit the criteria for nutritional rickets may require urine studies, specialised hormone testing or genetic investigations.

How is Rickets Treated and Managed?

Treatment depends on the specific cause of rickets. Vitamin D and calcium treatments are appropriate for nutritional deficiency, but other forms require different treatment.

Common treatment and management approaches of rickets are given below:

  1. Nutritional Rickets Rickets caused by vitamin D or calcium deficiency is treated by correcting the deficiency. Vitamin D3 and adequate calcium intake may be prescribed according to the child's age, severity and blood test results.

  2. Vitamin D-Dependent Rickets Inherited disorders affecting vitamin D activation or response require specialist treatment. Depending on the specific disorder, treatment may include active vitamin D preparations such as calcitriol or other targeted therapy.

  3. Hypophosphataemic Rickets Phosphate-wasting disorders require treatment aimed at correcting phosphate imbalance. Management may include phosphate supplements, active vitamin D preparations or disease-specific medicines, depending on the underlying condition.

  4. Kidney-Related Rickets Children with chronic kidney or renal tubular disorders require treatment of the underlying kidney disease together with correction of calcium, phosphate and vitamin D abnormalities.

  5. Treatment of Malabsorption or Liver Disease When rickets results from poor nutrient absorption or abnormal vitamin D metabolism, treatment focuses on both the underlying condition and the resulting mineral deficiency.

  6. Orthopaedic Management Many leg deformities improve gradually after the underlying mineral problem is corrected and normal growth continues. Persistent or severe deformities may require assessment by an orthopaedic specialist. Surgery is generally considered only after metabolic treatment has been optimised.

Common Medicines Used to Treat Rickets

Medicines depend on the specific form of rickets. Common medicines that may be prescribed by doctors to treat rickets are given below:

  • Cholecalciferol: Vitamin D3 used for vitamin D-deficiency rickets.

  • Calcium Supplements: It can be used when dietary calcium intake is inadequate during treatment.

  • Calcitriol: An active form of vitamin D used in selected inherited or kidney-related forms rather than routine nutritional rickets.

  • Phosphate Supplements: May be prescribed in selected phosphate-wasting disorders under specialist supervision.

  • Disease-Specific Medicines: Some inherited forms of hypophosphataemic rickets may require targeted treatment under specialist supervision.

Note: Vitamin D, calcium, calcitriol and phosphate treat different metabolic abnormalities and should not be used interchangeably. Treatment should follow an appropriate diagnosis and medical advice.

Living With Rickets: Daily Challenges and Care

Children recovering from rickets may need temporary support with movement, daily activities and follow-up while normal mineralisation and skeletal development improve.

Some of the challenges and essential care points for rickets patients are listed below:

  1. Challenges
    • Walking Difficulties: Bowed legs, knock knees or muscle weakness can affect walking.
    • Delayed Motor Development: Younger children may take longer to sit, stand or walk.
    • Bone Discomfort: Physical activity may be uncomfortable in children with bone pain or weakness.
    • Growth Concerns: Height and skeletal development may need ongoing monitoring.
  2. Patient Well-Being
    • Follow Treatment Regularly: Vitamin D, calcium or other medicines should be given according to the prescribed schedule.
    • Support Safe Activity: Physical activity can usually increase gradually as strength and mineralisation improve.
    • Attend Follow-Up: Repeat examination, blood tests or X-rays may be needed to confirm healing and normal development.
  3. Expenses
    • Consultation Costs: Expenses may include paediatric, endocrine, nephrology or orthopaedic consultations.
    • Testing Costs: Blood tests, vitamin D testing and X-rays can contribute to the initial and follow-up costs.
    • Long-Term Care Costs: Inherited or treatment-resistant rickets may require specialised tests, genetic assessment and ongoing treatment.

What is the Prognosis for Rickets?

The prognosis for nutritional rickets is usually favourable when vitamin D or calcium deficiency is recognised and treated early. Blood test abnormalities generally improve first, while skeletal changes take longer to heal. As children still have significant growth ahead of them, some leg deformities can improve as normal mineralisation resumes.

Long-standing or severe deformities may persist and require orthopaedic assessment. In inherited, renal or metabolic forms, the long-term outlook depends on the underlying disorder and response to treatment.

How Can I Prevent Rickets?

Not all forms of rickets can be prevented, particularly those caused by inherited, kidney-related or metabolic disorders. However, the risk of some forms can be reduced by supporting healthy bone development and addressing nutritional or medical problems early.

Some preventive measures for rickets are given below:

  • Ensure children receive enough vitamin D and calcium for their age.

  • Provide vitamin D supplements when recommended, particularly during infancy or when deficiency risk is high.

  • Include calcium-rich foods as part of a balanced diet.

  • Encourage safe and appropriate sunlight exposure to support vitamin D production.

  • Identify and treat conditions that affect the absorption or metabolism of vitamin D, calcium or phosphate.

  • Monitor children taking long-term medicines that can interfere with bone or mineral metabolism.

  • Attend regular health checks when a child has kidney, liver, intestinal or inherited conditions that increase the risk of rickets.

Rickets Treatment Cost in India

Treatment costs vary according to whether a child has uncomplicated nutritional rickets or requires specialist investigation for an inherited, kidney-related or phosphate-wasting condition.

An overview of the approximate costs of rickets treatment in India is provided in the table below:

Treatment Component Approximate Cost in India
Paediatric or paediatric endocrinology consultation ₹500 - ₹2,000 per visit
25-OH vitamin D test ₹500 - ₹2,700
Calcium test ₹100 - ₹300
Phosphate test ₹150 - ₹550
Alkaline phosphatase test ₹100 - ₹300
PTH test, when required ₹1,500 - ₹2,000
X-ray of wrist, knee or affected bones ₹500 - ₹2,000
Vitamin D treatment ₹100 - ₹500
Calcium supplements ₹100 - ₹500 per month
Additional metabolic or genetic testing ₹15,000 - ₹30,000

Note: These are indicative prices rather than fixed charges. Costs may vary depending on the hospital, location and treatment required. For more accurate estimates, consult a hospital representative.

Does Health Insurance Cover Rickets in India?

Yes, health insurance provides coverage for rickets. Most uncomplicated nutritional rickets is managed through outpatient consultations, blood tests and medicines. These expenses are covered under a mediclaim policy only if it includes the OPD benefit.

If rickets requires a medically necessary admission for severe complications or surgery for a persistent deformity, the insurance company will pay for the expenses as per the policy terms and conditions. However, a waiting period may apply before a claim can be raised.

Make sure to review the coverage, exclusions, co-payments, sub-limits and other conditions before filing claims.

How Much Health Insurance Coverage is Needed for Rickets?

There is no fixed disease-specific sum insured recommended for rickets, as uncomplicated nutritional rickets is usually treated through relatively low-cost outpatient care.

A health insurance cover of around ₹5 - ₹10 lakh may meet basic hospitalisation needs for rickets treatment. A higher coverage of ₹15 - ₹20 lakh can offer broader protection against major hospitalisation, surgery or other healthcare expenses resulting from inherited or chronic metabolic rickets.

FAQs

  • Q1. At what age can rickets develop?

    Ans: Rickets can affect infants, children and adolescents while their growth plates remain open.
  • Q2. Is rickets contagious?

    Ans: No. Rickets cannot spread from one child to another.
  • Q3. Can a breastfed baby develop rickets?

    Ans: Yes. Infants with vitamin D deficiency can develop rickets if they do not receive an adequate source of vitamin D. This is why preventive supplementation is commonly advised.
  • Q4. Can a child have rickets with a normal vitamin D level?

    Ans: Yes. Rickets can develop from calcium deficiency, phosphate loss, kidney disease or inherited metabolic disorders even when vitamin D levels are adequate.
  • Q5. Does rickets always cause bowed legs?

    Ans: No. Rickets symptoms can vary with age and may include skull changes, muscle weakness, delayed growth or widened wrists before leg deformities appear.
  • Q6. Can rickets affect a child's teeth?

    Ans: Yes. Rickets can cause delayed tooth eruption and enamel abnormalities in some children.
  • Q7. Can rickets delay walking?

    Ans: Yes. Muscle weakness and skeletal changes occurring due to rickets can delay standing or walking.
  • Q8. Can rickets cause seizures?

    Ans: Yes. Severe calcium deficiency associated with some forms of rickets can cause seizures.
  • Q9. Does every child with vitamin D deficiency have rickets?

    Ans: No. Vitamin D deficiency increases the risk, but rickets involves characteristic abnormalities of growing bones and growth plates.
  • Q10. Can rickets be diagnosed with a vitamin D test alone?

    Ans: No. Diagnosis of rickets usually requires clinical assessment, blood tests and characteristic X-ray findings.
  • Q11. Can rickets cause bone fractures?

    Ans: Yes. Poor mineralisation due to rickets can weaken growing bones and increase fracture risk.
  • Q12. Why is alkaline phosphatase tested in rickets?

    Ans: Alkaline phosphatase is usually elevated in active rickets and helps assess abnormal bone mineralisation.
  • Q13. Can rickets be inherited?

    Ans: Yes. Some inherited forms of rickets are known to cause imbalance in vitamin D metabolism or phosphate regulation.
  • Q14. Is sunlight enough to treat rickets?

    Ans: No, sunlight is not enough to treat rickets. Treatment depends on the underlying cause of rickets and may require vitamin D, calcium, phosphate or other specific therapy.
  • Q15. Do leg deformities caused by rickets always require surgery?

    Ans: No. Many deformities caused by rickets improve after the underlying cause is treated. Surgery may be considered if significant deformity persists.
  • References

    • https://pubmed.ncbi.nlm.nih.gov/34969941/

    • https://pmc.ncbi.nlm.nih.gov/articles/PMC9307538/

    • https://pmc.ncbi.nlm.nih.gov/articles/PMC9395459/

    • https://pmc.ncbi.nlm.nih.gov/articles/PMC11541088/

    • https://pubmed.ncbi.nlm.nih.gov/36604939/

    • https://pmc.ncbi.nlm.nih.gov/articles/PMC11189282/

Other Health Disease Pages