The importance of insulin‐like growth factor I (IGF‐I) for growth is well established. However, the lack of IGF‐I on the skeleton has not been examined thoroughly. Therefore, we analyzed the structural properties of bone from mice rendered IGF‐I deficient by homologous recombination (knockout [k/o]) using histomorphometry, peripheral quantitative computerized tomography (pQCT), and microcomputerized tomography (μCT). The k/o mice were 24% the size of their wild‐type littermates at the time of study (4 months). The k/o tibias were 28% and L1 vertebrae were 26% the size of wild‐type bones. Bone formation rates (BFR) of k/o tibias were 27% that of the wild‐type littermates. The k/o bones responded normally to growth hormone (GH; 1.7‐fold increase) and supranormally to IGF‐I (5.2‐fold increase) with respect to BFR. Cortical thickness of the proximal tibia was reduced 17% in the k/o mouse. However, trabecular bone volume (bone volume/total volume [BV/TV]) was increased 23% (male mice) and 88% (female mice) in the k/o mice compared with wild‐type controls as a result of increased connectivity, increased number, and decreased spacing of the trabeculae. These changes were either less or not found in L1. Thus, lack of IGF‐I leads to the development of a bone structure, which, although smaller, appears more compact.