Rickets is a childhood condition characterized by the softening and weakening of bones due to impaired mineralization of the growth plates. This failure to properly deposit calcium and phosphate leads to skeletal deformities. Treatment focuses on correcting the underlying mineral imbalance and addressing any physical damage. The specific course of action depends on whether the cause is a simple nutritional lack or a more complex genetic or metabolic disorder.
Standard Nutritional Treatment
Nutritional rickets, the most common form, is primarily caused by a deficiency in Vitamin D, calcium, or phosphate intake. Treatment involves a high-dose regimen of Vitamin D to rapidly restore the body’s stores. The typical dose is 2,000 International Units (IU) per day for at least three months, though some protocols use a single dose up to 600,000 IU.
This therapy must be paired with adequate calcium intake, as both are necessary for bone remineralization. Children usually receive a daily oral calcium supplement of at least 500 milligrams (mg). This intensive phase aims to quickly correct the metabolic defect, allowing growth plates to close and bone tissue to harden. Once biochemical healing is confirmed, the child transitions to a long-term maintenance dose of 400 to 600 IU daily to prevent recurrence.
Treating Non-Nutritional Forms
Rickets can also be caused by genetic or chronic diseases that prevent the body from properly processing minerals, even with adequate intake. These non-nutritional forms, such as X-linked hypophosphatemic rickets (XLH) or renal rickets, require specialized, lifelong medical management.
For XLH, the conventional approach combines oral phosphate supplements with an active form of Vitamin D, such as calcitriol. While this regimen improves bone mineralization, it carries a risk of complications like kidney stone formation. A newer, targeted therapy for XLH is burosumab, a monoclonal antibody that inhibits the hormone Fibroblast Growth Factor 23 (FGF23). Burosumab is often considered superior to conventional therapy because it more effectively improves rickets severity and growth with fewer adverse effects.
Management of Skeletal Deformities
While medical treatment corrects the underlying cause, physical interventions are often necessary to address existing skeletal deformities, such as bowed legs (genu varum) or knock-knees (genu valgum). For mild deformities in young children, spontaneous bone remodeling after successful medical therapy may be sufficient for correction. Non-surgical approaches, including physical therapy and the use of braces or orthotics, can support the limbs and encourage straighter alignment.
Surgical intervention is reserved for severe deformities that persist or worsen after the metabolic condition is controlled and the growth plates are no longer active. The most common procedure is a corrective osteotomy, where the affected bone is cut and realigned. In some cases, a technique called guided growth may be used, which involves temporarily slowing growth on one side of a bone to gradually correct alignment over time.
Monitoring Treatment Progress and Recovery
Monitoring is a continuous process used to confirm healing and fine-tune the treatment dosage. Healthcare providers use laboratory tests and imaging to track the body’s response. Blood tests regularly measure levels of calcium, phosphate, and the storage form of Vitamin D (25-hydroxyvitamin D).
A key indicator of healing is the normalization of alkaline phosphatase, an enzyme typically elevated in active rickets due to increased bone cell activity. X-rays of the wrist or knee are essential for radiological follow-up. Healing is confirmed when the characteristic widening and cupping of the growth plates, known as the “rickets line,” disappears and normal bone mineralization is visible. While blood markers often recover within weeks, radiographic evidence of complete healing and resolution of deformities can take several months.