Rickets is a disease entity that was first described more than 2,000 years ago, and it is often mistakenly considered a diagnosis of the past or of developing countries. There has been a recent resurgence of this disease in the United States and Europe. The United States did witness the eradication of nutritional rickets when it was discovered in the 1930s that vitamin D was antirachitic. It is difficult to ascertain the current prevalence of this condition due to the lack of ongoing national surveillance. Current estimates of the prevalence of nutritional rickets range from 5 to 9 per 1,000,000 children aged 6 months to 5 years.

In general terms, rickets results from the failure of bone to mineralize. Calcification of the cartilaginous growth plate is delayed in children whose epiphyses have yet to fuse. It is usually delayed due to an inadequate supply of calcium or phosphate to the growth plate. The causes of rickets can be grouped into three categories: (a) inability to maintain serum calcium-calcipenic, (b) inability to maintain serum phosphorus-phosphonpenic, and (c) causes that inhibit mineralization of the growth plate and osteoid. Vitamin D-deficiency rickets is a calcipenic form of rickets, as well as any abnormalities of vitamin D metabolism. The many forms of impaired renal phosphate reabsorption are included as phosphopenic types of rickets. Vitamin D is a prohormone and has two sources: cholecalciferol and ergocalciferol. When the skin is exposed to ultraviolet light, 7-dehydrocholesterol is converted into cholecalciferol (vitamin D₃). Ergocalciferol or vitamin D₂ is obtained from the diet. Vitamin D is hydroxylated in the liver to 25-hydroxyvitamin D, and then in the kidney, 25-hydroxyvitamin D is hydroxylated to 1,25 dihydroxyvitamin D. 1,25-dihydroxyvitamin D, or calcitriol, ensures

adequate absorption of calcium from the intestines and meets the requirements of a growing child.