Epidemiology

In a community-based population in the US, the incidence of nutritional rickets in children younger than 3 years was 24.1 per 100,000 for the decade beginning in 2000.[8] Nutritional rickets is associated with black and South Asian ethnicity, and with breastfeeding.[4][8]​​[9][10]​​ The peak incidence of rickets is between 6 and 23 months, with a further peak among adolescents aged 12 to 15 years.[11]

Globally, nutritional deficiencies are the leading cause of rickets, followed by vitamin D-dependent, vitamin D-resistant, and renal rickets. Surprisingly, in the sunniest areas of the world, rickets is still a major health problem. Reasons for this may include sociocultural factors (such as burka-wearing practices, an increase in sedentary lifestyles, less time spent outdoors), foods unfortified with vitamin D, and diets low in calcium.[12][13] Increased skin pigmentation is associated with reduced capacity to synthesise colecalciferol. Increased sunscreen use has also been implicated in vitamin D deficiency.[14]

Of the genetic causes of rickets, the most common is X-linked hypophosphataemic rickets, with a prevalence of 1 in 20,000.[6] The prevalence of X-linked hypophosphataemic rickets is estimated to be between 16 per million and 50 per million.[6][15] In children presenting with a new diagnosis of rickets, vitamin D deficiency and X-linked hypophosphataemic rickets are diagnosed at similar rates. Other genetic causes (mutations in vitamin D 25-hydroxylase or 1-alpha-hydroxylase enzymes or in the vitamin D receptor, or autosomal dominant and autosomal recessive hypophosphataemic rickets) are very rare.

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