Other meanings of Rickets
Medicine
Rickets is a childhood disease characterized by softening and weakening of bones, typically caused by severe vitamin D deficiency, leading to impaired mineralization of the growing skeleton.1 It results in bone pain, delayed growth, and skeletal deformities such as bowed legs and a protruding breastbone. The condition is most common in children aged 6 to 36 months, when bone growth is rapid. While historically a major public health problem in industrialized nations, rickets has re-emerged in some communities due to inadequate sun exposure and dietary deficiencies.2
Rickets arises from a failure of chondrocytes and osteoblasts to mineralize newly formed bone matrix, leading to an accumulation of unmineralized osteoid.1 The primary cause is vitamin D deficiency, which reduces intestinal absorption of calcium and phosphate, resulting in hypocalcemia and secondary hyperparathyroidism. Less commonly, rickets can be caused by hereditary disorders such as X-linked hypophosphatemic rickets, which involves renal phosphate wasting, or by dietary calcium deficiency even with adequate vitamin D.3 In rare cases, it may be due to renal tubular acidosis or liver disease that impairs vitamin D activation.
Children with rickets often present with delayed fontanelle closure, craniotabes (soft skull bones), and a rachitic rosary—beading at the costochondral junctions.4 Other signs include Harrison's sulcus, a horizontal groove along the lower ribs, and bowing of the legs (genu varum) or knock-knees (genu valgum). Diagnosis is based on clinical examination, radiographs showing cupping and fraying of the metaphyses, and laboratory findings of low serum phosphate, elevated alkaline phosphatase, and low 25-hydroxyvitamin D levels.1 In severe cases, hypocalcemia can cause seizures or tetany.
Treatment involves high-dose oral vitamin D (typically 1,000–4,000 IU daily) and calcium supplementation, with monitoring of serum calcium and urinary calcium excretion to avoid hypercalcemia. Most children respond within weeks, with radiographic healing visible in 2–4 weeks. Prevention relies on adequate sun exposure, vitamin D supplementation for breastfed infants, and fortification of foods such as milk and cereals. In the United States, the American Academy of Pediatrics recommends 400 IU daily for all infants and children.2 For hereditary forms, specific treatments like phosphate supplementation are required.
Beyond the classic deficiency, rickets has historical and cultural dimensions. In the 17th century, it was called the "English disease" due to its prevalence in industrialized cities with smog, which blocked ultraviolet radiation.5 The discovery of vitamin D and its role in rickets led to the fortification of milk in the 1930s, nearly eradicating the disease in the US. However, rickets persists in some populations, including dark-skinned individuals living at high latitudes and infants exclusively breastfed without supplementation.2 A rare form, vitamin D-dependent rickets type I, is caused by mutations in the CYP27B1 gene, which encodes the enzyme that activates vitamin D.3 Additionally, some studies suggest that maternal vitamin D deficiency during pregnancy increases the risk of rickets in offspring, highlighting the importance of prenatal nutrition.
This article focuses on the classic nutritional form of rickets; hereditary forms are mentioned but not covered in depth.
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