Kyphosis, an idiopathic disease, occurs in swine and humans. We induced kyphosis by altering maternal dietary vitamin D (D) and pig dietary D, Ca and P. The objective was to characterize bone traits and gene expression in the kyphosis model and assess maternal carryover effects. Traits from mechanical tests to characterize femur integrity are reported herein. Sows were fed diets with 0, 325 or 1750 IU D/kg (n = 6, 8, or 9/diet). At weaning (23 ± 2 d) pigs were fed diets with 0 (-D) or 280 (+D) IU D/kg, each with 95% (95P) or 120% (120P) of the P requirement. Pigs were killed at birth (n = 23), weaning (n = 22), and at the end of nursery (n = 185) for bone and tissue analysis. Excised femurs were subjected to a 4-point bending test to determine bending moment (BM), stress, strain, and modulus of elasticity (ME) at the yield point of load deformation curves. Mass moment of inertia (MOI) was derived from CT scans. ME encompasses of BM, stress, strain and MOI and is assumed to be a constant property of a material. No differences in ME were detected at birth. At weaning ME increased in pigs produced by sows fed 1750 (P < 0.05). At the end of nursery ME depended on maternal diets (interaction, P < 0.05). ME increased in pigs fed +D95P if produced by sows fed 0 or 325 but decreased if produced by sows fed 1750. As previously reported, DXA whole body bone mineral density also indicated maternal carryover effects, but the pattern differed among diets. Therefore whole body bone and femur integrity traits differ, but provide unique characterization of the model. As previously reported, the kyphosis model was further characterized by molecular analysis of bone and D homeostatic cell signaling mechanisms. All traits contribute to the characterization of the kyphosis model but a specific mechanism by which the deformity is induced has yet to be determined.