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Healing of rachitic lesions in chicks by 24R,25‐dihydroxycholecalciferol administered locally into bone
Author(s) -
Lidor Cobi,
Atkin Isaac,
Ornoy Asher,
Dekel Samuel,
Edelstein Samuel
Publication year - 1987
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.5650020203
Subject(s) - microgram , rickets , cholecalciferol , in vivo , endocrinology , vitamin d and neurology , medicine , metabolite , tibia , cartilage , vitamin , active metabolite , chemistry , biology , anatomy , in vitro , biochemistry , microbiology and biotechnology
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) 2 D 3 in vivo to D‐deficient chicks resulted in disappearance of the rachitic lesions in the same leg. Administration of 1 μg 1,25(OH) 2 D 3 in a similar manner failed to show any sign of healing. Injection of 5 μg 25(OH)D 3 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) 2 D 3 failed to reverse the rachitic lesions and induced only minimal recovery. These findings suggest that 24,25(OH) 2 D 3 at the higher doses has a direct local effect on cartilage and bone, while 1,25(OH) 2 D 3 has no such effect in chicks. 25(OH)D 3 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.