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Rickets is a condition of growing children in which there is failure of normal mineralisation of the epiphyseal growth plate. Normal growth plate development is dependent upon a cascade of events that consists of resting chondrocytes becoming preproliferative, proliferative, hypertrophic and finally apoptotic, which is a signal for the invasion of the growth plate by bone-forming cell precursors that replace the apoptosed cartilage cells with bone cells that mineralise the epiphyseal growth plate into true bone. Eventually, the growth plate is obliterated as the metaphyseal and epiphyseal ends of the bones fuse. It is therefore evident that rickets can only occur in growing children in whom the growth plate is still not fused.
The final step of apoptosis is promoted by phosphate which has to be present in sufficient concentration to facilitate apoptosis1. In the absence of enough phosphate, apoptosis does not proceed correctly, the growth plate widens and there is failure of normal invasion of bone-forming cell precursors. This results in the typical radiological appearances of rickets.
Thus, it can be seen that any cause of hypophosphataemia may be associated with the development of rickets. Primary hypophosphataemic disorders are usually associated with raised Fibroblast Growth Factor 23 (FGF23) and normal parathyroid hormone (PTH) concentrations. By contrast, secondary hypophosphataemia is caused by relative calcium deficiency resulting from inadequate absorption either because of vitamin D deficiency, or because of an absolute deficiency of calcium in the diet, both of which …
Contributors Both authors have contributed equally to this manuscript.
Competing interests Dr Allgrove has received honoraria from Novartis and Alexion. Professor Mughal has received honoraria from Novartis, Alexion & Danone. Neither author has a conflict of interests.
Provenance and peer review Commissioned; internally peer reviewed.