Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Rickets is the clinical consequence of impaired mineralization of bone matrix throughout the growing skeleton in children, whilst osteomalacia is the result of this disturbance after the growth plates have fused in adults. The three major causes of rickets and osteomalacia are vitamin D deficiency, renal tubular dysfunction, and abnormalities of chondrocyte, osteoblast or bone matrix function. Rickets and osteomalacia can occur as heritable disorders. The major clinical features of rickets and osteomalacia include bone pain and tenderness, skeletal deformity, muscle weakness and occasionally tetany due to hypocalcaemia. Hypocalcaemia, hypophosphataemia, and raised serum alkaline phosphatase activity are typically found together with radiographic abnormalities such as widening of growth plates in rickets and pseudofractures in osteomalacia. Serum 25-hydroxyvitamin D concentrations are low in states of vitamin D deficiency, but may be normal in chronic renal failure, hereditary forms of rickets and oncogenous osteomalacia; in these latter disorders, the serum 1,25-dihydroxy vitamin D concentrations are low or inappropriately in the normal range. Treatment with vitamin D, or its active metabolites, will generally provide relief of bone pain, improve mobility and prevent fractures, but must be carefully monitored. © 2009 Elsevier Ltd. All rights reserved.

Original publication




Journal article



Publication Date





483 - 488