In the first stage of the base excision repair pathway the enzyme uracil DNA glycosylase (UNG) recognizes and excises uracil (U) from DNA filaments. U repair is believed to occur via a multistep base-flipping process, through which the damaged U base is initially detected and then engulfed into the enzyme active site, where it is cleaved. The subtle recognition mechanism by which UNG discriminates between U and the other similar pyrimidine nucleobases is still a matter of active debate. Detailed structural information on the different steps of the base-flipping pathway may provide insights on it. However, to date only two intermediates have been trapped crystallographically thanks to chemical modifications of the target and/or of its complementary base. Here, we performed force-field based molecular dynamics (MD) simulations to explore the structural and dynamical properties of distinct UNG/dsDNA adducts, containing A:U, A:T, G:U, or G:C base pairs, at different stages of the base-flipping pathway. Our simulations reveal that if U is present in the DNA sequence a short-lived extra-helical (EH) intermediate exists. This is stabilized by a water-mediated H-bond network, which connects U with His148, a residue pointed out by mutational studies to play a key role for U recognition and catalysis. Moreover, in this EH intermediate, UNG induces a remarkable overall axis bend to DNA. We believe this aspect may facilitate the flipping of U, with respect to other similar nucleobases, in the latter part of the base-extrusion process. In fact, a large DNA bend has been demonstrated to be associated with a lowering of the free energy barrier for base-flipping. A detailed comparison of our results with partially flipped intermediates identified crystallographically or computationally for other base-flipping enzymes allows us to validate our results and to formulate hypothesis on the recognition mechanism of UNG. Our study provides a first ground for a detailed understanding of the UNG repair pathway, which is necessary to devise new pharmaceutical strategies for targeting DNA-related pathologies.