As a result of vitamin D deficiency, calcium deficiency, or phosphate deficiency, rickets can cause soft, weak bones in children. Here, we explore the causes, symptoms, diagnosis, treatment, and prevention of rickets, which can result in bone deformities, growth retardation, and other complications.
The primary cause of rickets is a deficiency in vitamin D, which plays a crucial role in calcium and phosphate metabolism and bone health. In addition to inadequate sunlight exposure, inadequate dietary intake of vitamin D, calcium, or phosphate, malabsorption disorders, certain medications, and genetic conditions that affect vitamin D metabolism, rickets can also be caused by deficiencies in these nutrients.
Signs and symptoms of rickets may vary depending on the severity and duration of the deficiency.
Growth and development are delayed
Bones that are soft, weak, or deformed, leading to bowed legs, knock knees, or pigeon chests
Weak muscles and decreased muscle tone
Especially in the arms, legs, spine, or pelvis, bone pain or tenderness can occur
Teething delays or dental abnormalities such as enamel defects or delayed eruption of teeth
An increased risk of fractures or deformities, especially under stress or weight-bearing exercise
The diagnosis of rickets involves a combination of medical history, physical examination, laboratory tests, and imaging studies. Diagnostic procedures include:
It is important to tell your healthcare provider about your symptoms, dietary habits, sun exposure, and family history of rickets or other bone disorders.
A thorough physical examination of the child's skeletal system can identify signs of rickets, including bone deformities, muscle strength, and range of motion.
Tests for vitamin D, calcium, phosphate, alkaline phosphatase, and parathyroid hormone can detect deficiencies or abnormalities associated with rickets in the blood.
To diagnose rickets, X-rays or bone density scans may be used to evaluate bone density, bone structure, and detect characteristics associated with the disease, such as widening of growth plates, fractures, and bone deformities.
The goal of rickets treatment is to correct the underlying vitamin D, calcium, or phosphate deficiency and promote bone health and development.
The use of oral vitamin D supplements, such as cholecalciferol (vitamin D3) or ergocalciferol (vitamin D2), may be prescribed to replenish deficient vitamin D levels and restore normal calcium and phosphate metabolism.
Supplementation with calcium and phosphate may be recommended in cases of severe calcium or phosphate deficiencies.
Getting enough sunlight, particularly in the early morning or late afternoon when UV radiation is less intense, can stimulate the skin's production of vitamin D.
Increasing consumption of vitamin D-rich foods, such as fatty fish, fortified dairy products, eggs, and mushrooms, as well as calcium and phosphate-rich foods, such as dairy, leafy greens, nuts, and seeds, can promote bone health.
A regular monitoring of vitamin D, calcium, and phosphate levels, as well as bone health assessments, may be recommended to track progress and adjust treatment.
Vitamin D, calcium, and phosphate intake must be adequate through diet, sunlight exposure, and supplementation as needed to prevent rickets. Other preventive measures may include:
The most effective way to prevent rickets is to encourage breastfeeding and to provide vitamin D supplements to breastfed infants. Breastmilk is a natural source of vitamin D and other nutrients essential for infant growth and development.
Foods fortified with vitamin D and calcium, such as milk, cereal, and orange juice, can help ensure adequate nutrient intake, especially for populations at risk.
Balancing sun exposure with sun safety practices, such as wearing protective clothing, hats, and sunscreen, can help prevent sunburns and skin damage while still allowing adequate vitamin D production.
