Deficiency of vitamin D metabolites results in vitamin D-resistant states. Rickets and osteomalacia may occur when the supply of vitamin D is inadequate, its metabolism is abnormal, or tissues are resistant to its action. Categorizing rickets and osteomalacia by etiology is important in relation to the manifestations of disease and to effective treatment. In children, changes include defective calcification of growing bone and hypertrophy of the epiphyseal cartilages. Epiphyseal cartilage cells cease to degenerate normally, but new cartilage continues to form, so that the epiphyseal cartilage becomes irregularly increased in width.
Calcification then stops, and osteoid material accumulates around the capillaries of the diaphysis.
The cancellous bone of the diaphysis and cortical bone may be resorbed in chronic deficiency. Adequate treatment with vitamin D permits calcium and phosphate deposition through degeneration of the cartilage cells within 24 h and penetration by a vascular network within 48 h. Osteoid material at the diaphysis ceases to form, and normal endochondral production of new bone is resumed. In adults, the changes are similar but are not confined to the ends of the long bones. Symptoms and Signs Maternal osteomalacia can lead to metaphyseal lesions and tetany in the newborn. Young infants are restless and sleep poorly.