This chapter reviews the general features of rickets, classification of the various causes of the disease, and nutritional rickets. Rickets is a clinical syndrome characterized by a failure of or delays in endochondral calcification at the growth plates of long bones, resulting in deformation of the growth plate, a reduction in longitudinal growth and the development of bone deformities. The disease is also associated with osteomalacia, which is a failure of mineralization of preformed osteoid on the trabecular and cortical bone surfaces of all bones. Rickets has been a public health problem for children living in temperate climates for many centuries. The causes of rickets may be divided into three major categories based on their pathogenetic mechanisms. Normal mineralization of the growth plate and of osteoid at the trabecular and cortical bone surfaces is dependent on a number of different factors, including the presence of normal concentrations of both calcium and phosphorus, and of alkaline phosphatase. The classification helps to categorize the causes into broad groups, each of which has characteristic biochemical changes, which help in establishing the pathogenesis of the disease in an individual child. In the calciopenic forms of rickets, the typical biochemical changes include hypocalcemia and hyperparathyroidism, while in the phosphopenic form, hypophosphatemia with normal parathyroid hormone concentrations are characteristic and in many situations associated with elevated fibroblast growth factor 23 (FGF-23) concentrations.