The skin is the largest organ in the body and protects internal organs from external insults. When the skin is wounded, the tissue responds rapidly to restore barrier function. One critical step of wound healing is epithelialization, in which epidermal cells called keratinocytes proliferate and migrate collectively to repair the lesion. To drive and coordinate movement, keratinocytes form adhesions to their neighboring cells and to the extracellular matrix (ECM). In this chapter, we summarize the current knowledge of two main classes of cell adhesion molecules in the context of wound epithelialization: cadherins, which mediate cell-cell adhesion, and integrins, which mediate cell–ECM adhesion. We draw from studies in diverse organisms, including Drosophila, C elegans, Xenopus, mice, and humans, to build a consensus understanding of how these adhesions drive coordinated epidermal migration. Cadherins mediate cell–cell adhesion and enable transmission of cytoskeletal forces between cells. Cadherins are initially downregulated at the wound edge to facilitate cell movement, then reinforced at focal sites to enable coordinated migration. Integrins mediate cell–ECM adhesion and are critical for generating traction forces that drive migration. During wound healing, integrin expression changes to interact with the provisional wound matrix, and integrins relocalize to contribute to cell-cell adhesion. Cadherin and integrin adhesions dynamically remodel in space and time and undergo complex crosstalk with each other and other adhesion structures. Understanding these molecular mechanisms by harnessing diverse model organisms and systems is necessary for developing novel therapeutic strategies to improve wound healing and prevent chronic wounds.