Wound healing studies both in vitro and in vivo have received a lot of attention recently. In vivo wound healing is a multi-step process involving physiological factors such as fibrinogen forming the clot, the infiltrated inflam-matory cells, the recruited fibroblasts and the differentiated myofibroblasts as well as deposited collagens. All these actors play their roles at different times, aided by a cascade of morphogenetic agents and the result for the repair is approximatively successful but the imperfection is remained for large scars with fibrosis. Here, we want to study wound healing from the viewpoint of skin biomechanics, integrating the particular layered geometry of the skin, and the role of the neighbouring wound epidermis. After 2 days post-injury, it migrates towards the wound centre to cover the hole, the migration being coupled to proliferation at the wound border. Such a process is dominated by the skin properties which varies with ages, locations, pathologies, radiations, etc. It is also controlled by passive (actin, collagen) and active (myo-fibroblasts) fibres. We explore a growth model in finite elasticity of a bilayer surrounding a circular wound, only the interior one being proliferative and contractile. We discuss the occurrence of an irregular wound geometry generated by stresses and show quantitatively that it results from the combined effects of the stiffness, the size of the wound, eventually weakened by actin cables. Comparison of our findings is made with known observations or experiments in vivo.