The anatomic discontinuity of the skin caused by physical, chemical, or thermal insult is restored by a mechanism of partial regeneration. Wound healing is an orderly, integrated, dynamic process comprised of multiple temporally and spatially overlapping but distinct phases, namely inflammation, vascularization, fibroplasia, reepithelialization, and remodeling. The biological signals released during the initial clot formation and throughout the repair modulate controlled migration, proliferation, and differentiation of cells actively involved in. this event leading to wound closure. This process is completed by the synthesis of extracellular matrix proteins in appropriate quantity and quality. Considerable advances made in understanding cell-cell and cell-matrix interactions in cutaneous wound healing provide evidence for a critical role of matrix in influencing cell migration, polarity, and orientation. The formation of surface epithelium to close the wound is precisely orchestrated with the underlying dermal repair. This synchrony is key to preventing either insufficient or excess wound repair. Though the importance of communication between the layers of skin-epidermis and dermis-is well realized, the mechanism underlying this marvelous event needs in-depth study. Communication must occur between diverse cell types, many of which are only transiently present, to recreate a structure that is formed predominantly by cells derived from diverse embryological origin, the epidermis from the ectoderm, and the dermis from the mesodermal mesenchyme. This review focuses on the basic mechanisms underlying the interaction of dermal matrix with surface epithelial layer to facilitate normal wound healing.