Skip to content

What Causes Rickets in Adults?: Understanding Osteomalacia

5 min read

According to the National Institutes of Health, an estimated 1 billion people worldwide have a vitamin D deficiency, the primary culprit behind the adult form of rickets. This article explores what causes rickets in adults, medically known as osteomalacia, detailing how it affects bone health and what steps can be taken for prevention and treatment.

Quick Summary

Adult rickets, or osteomalacia, results from impaired bone mineralization due to deficiencies in vitamin D, calcium, or phosphate. It can also stem from malabsorption syndromes or liver/kidney disease. The condition causes bones to become soft and weak.

Key Points

  • Adult Rickets is Osteomalacia: In adults, the condition is called osteomalacia, which means 'soft bones,' as their growth plates have already fused.

  • Vitamin D is Crucial: The most common cause is vitamin D deficiency, which is necessary for absorbing calcium and phosphate for strong bones.

  • Beyond Nutritional Intake: Underlying conditions like malabsorption disorders (Celiac, Crohn's), liver disease, and kidney disease can impair nutrient absorption and metabolism.

  • Symptoms Differ from Childhood Rickets: Adult symptoms include persistent bone pain (especially in the hips and pelvis), muscle weakness, and increased fracture risk, rather than bowed legs.

  • Prevention is Possible: Ensuring adequate vitamin D through safe sun exposure, diet (oily fish, fortified foods), and supplements can prevent most cases.

In This Article

The Distinction: Rickets in Children vs. Osteomalacia in Adults

While the term 'rickets' is typically associated with children, the adult equivalent is known as osteomalacia, which literally means 'soft bones'. The fundamental problem is the same in both conditions: a failure of the bones to mineralize properly. However, because children's bones are still growing, rickets can lead to characteristic deformities like bowed legs and skeletal abnormalities. In adults, whose bones have finished growing, the signs are more commonly persistent bone pain, muscle weakness, and an increased risk of fractures. Understanding this distinction is the first step toward correctly identifying and treating the condition. A proper nutrition diet is central to both preventing and managing osteomalacia.

Primary Nutritional Causes

Vitamin D Deficiency

Vitamin D is essential for the body's absorption of calcium and phosphate from the intestines, which are the key minerals required for bone hardening. The most common cause of osteomalacia is a long-term deficiency of this vital nutrient.

  • Insufficient Sunlight Exposure: The skin naturally produces vitamin D when exposed to ultraviolet-B (UVB) light from the sun. Risk factors for inadequate sun exposure include living in high-latitude areas with less intense sunlight, working indoors during daylight hours, wearing clothing that covers most of the skin for cultural or religious reasons, and having darker skin pigmentation, which reduces UVB absorption.
  • Inadequate Dietary Intake: While sunlight is the main source, a diet lacking in vitamin D-rich foods can contribute to deficiency, especially in regions with limited sun exposure. Natural sources include oily fish (salmon, sardines), egg yolks, and fortified foods like milk, cereals, and orange juice.

Calcium or Phosphate Deficiency

Although less common in developed countries, a diet severely lacking in calcium can directly lead to osteomalacia. Phosphate deficiency is even rarer from diet alone, as phosphate is abundant in many foods, but can occur in certain conditions affecting absorption.

Underlying Medical Conditions

Even with adequate vitamin D and mineral intake, certain medical conditions can interfere with absorption or metabolism, leading to osteomalacia.

Malabsorption Syndromes

Conditions that affect the gut's ability to absorb nutrients can severely impact vitamin D uptake. These include:

  • Celiac Disease: An autoimmune disorder where the immune system reacts to gluten, damaging the small intestine's lining.
  • Crohn's Disease: A type of inflammatory bowel disease that causes chronic inflammation of the digestive tract.
  • Cystic Fibrosis: A genetic disorder causing the body to produce thick, sticky mucus that can block ducts and interfere with nutrient absorption.
  • Gastric Bypass Surgery: Altering the digestive tract can significantly reduce the absorption of fat-soluble vitamins, including vitamin D.

Liver and Kidney Disorders

Vitamin D is not active when first produced by the skin or ingested. It undergoes a two-step activation process, first in the liver and then in the kidneys.

  • Liver Disease: Conditions like cirrhosis can impair the liver's ability to perform the initial conversion of vitamin D to its semi-active form, 25-hydroxyvitamin D (calcidiol).
  • Kidney Disease: The kidneys are responsible for the final activation step, converting calcidiol to the fully active form, 1,25-dihydroxyvitamin D (calcitriol). Chronic kidney disease can cause a loss of this function.

Medications and Genetic Factors

Certain medications, like long-term anti-seizure drugs (e.g., phenytoin, phenobarbital), can interfere with vitamin D metabolism. Rare genetic disorders, such as hereditary hypophosphatemic rickets, can cause the kidneys to waste phosphate, leading to bone softening.

Symptoms and Diagnosis of Osteomalacia

Symptoms of osteomalacia can be subtle at first, often manifesting as generalized fatigue and pain. The most characteristic signs include:

  • Widespread bone pain: Most commonly in the pelvis, hips, lower back, and legs. The pain is often dull and achy and can worsen with weight-bearing or activity.
  • Muscle weakness: Particularly affecting the muscles in the thighs and upper arms, which can lead to difficulty walking, climbing stairs, or getting out of a chair.
  • Increased fracture risk: Weakened bones are more susceptible to fractures from minor trauma or stress.

Diagnosis involves a physical exam, a review of medical and dietary history, and blood tests to check levels of vitamin D, calcium, phosphate, and parathyroid hormone. X-rays and a bone density scan (DEXA) may also be used to confirm bone softening. A bone biopsy, while definitive, is rarely needed.

Comparison: Osteomalacia vs. Rickets

Feature Osteomalacia (Adults) Rickets (Children)
Age of Onset Adulthood, after growth plates close Childhood, during bone growth and development
Bone Mineralization Impaired mineralization of existing bones Impaired mineralization of growing bones and cartilage
Deformities No new growth plate deformities; older deformities may persist Bowed legs, skeletal deformities, soft skull bones
Symptoms Widespread bone pain, muscle weakness, increased fractures Bone pain, delayed growth, skeletal deformities, dental issues
Underlying Cause Vitamin D, calcium, or phosphate deficiency; malabsorption; liver/kidney issues Same causes as osteomalacia, but affects growing bones and cartilage
Diagnosis Blood tests, X-rays, DEXA scan, biopsy (rare) Physical exam, blood tests, X-rays

Treatment and Prevention

The most common treatment for osteomalacia is high-dose vitamin D and calcium supplementation, along with managing any underlying condition that affects nutrient absorption or metabolism. For nutritional osteomalacia, increasing dietary intake and getting moderate sun exposure are key.

Key steps for prevention and management include:

  • Dietary Adjustments: Increase consumption of fatty fish, egg yolks, and fortified milk, cereals, and juices. For vegans, fortified plant-based milk and cereals are crucial.
  • Sunlight Exposure: Moderate sun exposure helps the body produce its own vitamin D. Recommended duration varies, but 10–30 minutes several times a week is often suggested, avoiding peak hours to reduce skin cancer risk.
  • Supplementation: Individuals with limited sun exposure, dark skin, or underlying conditions may require oral vitamin D supplements, particularly during winter months in higher latitudes.

In cases caused by liver or kidney disease, special forms of vitamin D, like calcitriol, may be required, and regular monitoring by a doctor is essential. Timely and appropriate treatment can lead to significant improvement in symptoms and bone health, but it may take several months.

Conclusion

While many associate rickets with children, its adult equivalent, osteomalacia, can cause significant bone pain and weakness if left untreated. The primary cause is most often a long-term vitamin D deficiency, although other factors like inadequate calcium intake, malabsorption, and underlying liver or kidney disease can also play a role. By prioritizing a balanced diet, ensuring moderate sun exposure, and consulting a healthcare provider for any potential underlying issues, adults can effectively prevent and manage this condition. For more detailed information on bone health, consult reliable medical sources such as the National Institutes of Health (NIH).

Frequently Asked Questions

Rickets affects children whose bones are still growing, causing deformities like bowed legs. Osteomalacia is the adult form, affecting mature bone and typically causing bone pain, muscle weakness, and a higher risk of fractures.

Yes, osteomalacia can often be cured by addressing the underlying cause, typically through vitamin D and calcium supplementation, along with dietary changes. Symptom improvement can take several months.

Early signs are often subtle and non-specific, including generalized fatigue and a dull, aching pain in the bones. As it progresses, the pain becomes more noticeable, particularly in the lower back, hips, and legs.

Doctors diagnose osteomalacia using a combination of methods, including a physical exam, a review of medical and dietary history, and blood tests to check levels of vitamin D, calcium, and phosphate. X-rays and bone density scans may also be used.

Yes, older adults are at a higher risk, partly because the body's ability to produce and store vitamin D decreases with age. Those who are homebound or institutionalized also face increased risk due to limited sun exposure.

Yes, individuals with darker skin have more melanin, which acts as a natural sunscreen and reduces the skin's ability to produce vitamin D from sunlight. They require more sun exposure to produce the same amount of vitamin D as those with lighter skin.

Eating foods rich in vitamin D and calcium is crucial. This includes fatty fish (salmon, sardines), egg yolks, and fortified foods like milk, cereals, and certain juices. For vegans, fortified plant-based milk and cereals are essential.

References

  1. 1
  2. 2
  3. 3
  4. 4
  5. 5
  6. 6
  7. 7
  8. 8
  9. 9
  10. 10

Medical Disclaimer

This content is for informational purposes only and should not replace professional medical advice.