AbstractObjectivesCortical bone structure undergoes dynamic changes during appositional growth and is highly sensitive to mechanical, hormonal, and nutritional influences. Vitamin D deficiency rickets can significantly disrupt the normal mineralization of newly formed bone leading to compromised bone structure. Here, we document ontogenetic trends in femoral cortical bone area and porosity during early growth and examine how vitamin D deficiency during childhood may impact these parameters in a sample of children from post‐medieval London, UK.Materials and MethodsMicro‐CT scans of the femur were collected from a documented sample of 138 children aged from birth to 8.5 years who were grouped by the presence and stage of rickets. Cross‐sections were extracted at the midsection and area and porosity measurements recorded. A local regression (LOESS) was used to fit curves to the dataset of children without rickets, which were used as comparative baselines for children with active and healed rickets.ResultsCortical bone porosity was elevated in all children with active rickets most likely reflecting delayed mineralization of osteoid and increased resorption due to secondary hyperparathyroidism. Total subperiosteal area and cortical bone area were higher in children with healed rickets than children without rickets reflecting the mineralization of osteoid following recovery from the deficiency.DiscussionThe results demonstrate marked differences in cortical bone structure in children with rickets, which vary according to age and disease stage. This study illustrates the complex interaction between metabolic bone diseases and bone formation and the importance of considering ontogenetic changes in bone structure in the study of disease during childhood.