![]() Studies from Asia continue to report high prevalence rates of nutritional rickets in rural central Tibet, about 30% of children aged 0–5 years had at least one sign of nutritional rickets on clinical examination. However, nutritional rickets seems to be more common in low-and middle-income countries, especially the Indian subcontinent, Africa, and the Middle East. Today, case rate estimates of 2.9–27 per 100,000 individuals have been reported in the United States and Europe. In the United States, incidence estimates of nutritional rickets in the early 2000s was 24.1 per 100,000 compared with 2.2 per 100,000 in the early 1980s. Nutritional rickets remains the most common type globally, representing the most frequent cause of pediatric bone disease in the world. Despite a global estimate of rickets, incidence is limited because of the paucity of basic data such as vitamin D dietary intake, especially among children in non-industrialized countries, and recent reports indicate an increase in its prevalence. Rickets is still a common disease worldwide. This review delves into the various aspects of rickets, from pathogenesis to new therapeutic tools, in order to provide a complete and updated picture on this disease and of its appropriate management. Oral Pi supplementation is usually indicated for FGF23-independent phosphopenic rickets, whereas the conventional treatment of FGF23-dependent types of rickets includes a combination of Pi and activated vitamin D.Īn important development has been the introduction of burosumab, a human monoclonal antibody to FGF23, which has been approved for the treatment of XLHR in children one year and older. X-linked hypophosphatemic rickets (XLHR) is the most common cause of inherited Pi wasting, with an incidence of 3.9 per 100,000 live births. Hypophosphatemic rickets is a heterogeneous group of entities due to renal Pi wasting wherein fibroblast growth factor 23 (FGF23) often plays a major role. Management of heritable types of rickets associated with defects in vitamin D metabolism or activation involves the administration of vitamin D metabolites. Where prevention has not been effective, treatment with calcium and/or vitamin D supplementation is recommended. Prevention of this form of rickets is possible and includes either supplementation or food fortification with Ca and vitamin D and adequate sunlight exposure. The prevalence of nutritional rickets has substantially declined compared with the prevalence a century ago, but the condition has been re-emerging even in some well-resourced countries. ![]() Diagnosis is usually established by medical history, physical examination, biochemical tests, and radiography. īased on the biochemical predominant abnormalities, rickets was typically classified as calcipenic or phosphopenic, although evidence suggests hypophosphatemia as the leading pathogenetic denominator of all forms. It predominantly affects longer bones, leading to poor bone growth and typical rickets bony deformities such as bow-legs and knock-knees. Rickets is a bone disease characterized by abnormal serum calcium (Ca) and phosphate (Pi) levels that may cause the development of abnormalities in chondrocytes’ differentiation and maturation and, consequently, a defective mineralization of the growth plate. Recent reports indicate an increased incidence and prevalence of this disease in industrialized countries indeed, in the United Kingdom, an overall incidence of 7.5 per 100,000 children younger than five years of age has been reported in the early part of the 21st century. Rickets was first described as a specific condition in the mid-seventeenth century and still remains a frequent condition worldwide.
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