Healing of rachitic lesions in chicks by 24R,25‐dihydroxycholecalciferol administered locally into bone

In an attempt to further define the nature of the active metabolite in bone formation, a series of experiments were conducted whereby vitamin D metabolites were administered locally in vivo into the proximal epiphyseal growth plate of the tibiae of rachitic chicks. Local administration of 3 μg of 24,25(OH)₂D₃ in vivo to D‐deficient chicks resulted in disappearance of the rachitic lesions in the same leg. Administration of 1 μg 1,25(OH)₂D₃ in a similar manner failed to show any sign of healing. Injection of 5 μg 25(OH)D₃ was followed by recovery from rickets in both the injected right leg and in the vehicle‐injected left tibia, although the recovery was more pronounced in the injected leg. Lower doses of 0.3 or 1 μg 24,25(OH)₂D₃ failed to reverse the rachitic lesions and induced only minimal recovery. These findings suggest that 24,25(OH)₂D₃ at the higher doses has a direct local effect on cartilage and bone, while 1,25(OH)₂D₃ has no such effect in chicks. 25(OH)D₃ is probably absorbed from the epiphyses into the blood stream and converted into the active metabolites, which were indeed detected in the blood to exert its systemic effects.