Nutritional rickets: thoughts about pathogenesis

Ann Med. 1993 Aug;25(4):379-84. doi: 10.3109/07853899309147300.


The pathogenesis of nutritional rickets is not well-understood. While the etiologies include deficiencies of vitamin D, calcium (Ca) or phosphate (PO4), and perhaps aluminium toxicity, the role these nutrients play in the development of tissue level anomalies characteristic of rachitic cartilage and bone has yet to be defined. Reported alterations in the biochemistry of rachitic bone and cartilaginous matrix which could adversely affect mineralization and endochondral ossification are of questionable significance since the tissues mineralize rapidly when exposed to Ca and PO4 salts in vivo and in vitro. The low Ca and PO4 concentrations of the extracellular fluid (ECF) bathing rachitic cartilage and bone matrix suggest that local mechanisms operate to impair mineralization. In healing rickets, the Ca and PO4 content of these tissue fluids increases in the same time-frame it takes to experimentally remineralize the matrices. However, it is not certain what determines the Ca and PO4 content of the ECF. Cytokines which may play a role in the cellular regulation of Ca and PO4 and maintain processes which contribute to normal patterns of endochondral ossification could provide a mechanism common to the pathogenesis of rickets from a variety of causes.

Publication types

  • Review

MeSH terms

  • Animals
  • Calcification, Physiologic
  • Calcium / deficiency
  • Calcium / metabolism
  • Disease Models, Animal
  • Humans
  • Hypocalcemia / complications
  • Hypocalcemia / metabolism
  • Hypophosphatemia / complications
  • Hypophosphatemia / metabolism
  • Infant, Newborn
  • Nutrition Disorders / complications*
  • Nutrition Disorders / metabolism
  • Nutrition Disorders / pathology
  • Phosphates / deficiency
  • Phosphates / metabolism
  • Rickets / etiology*
  • Rickets / metabolism
  • Rickets / pathology
  • Risk Factors
  • Vitamin D Deficiency / complications


  • Phosphates
  • Calcium