The anatomic discontinuity of the skin caused by physical, chemical, or the
rmal insult is restored by a mechanism of partial regeneration. Wound heali
ng is an orderly, integrated, dynamic process comprised of multiple tempora
lly and spatially overlapping but distinct phases, namely inflammation, vas
cularization, fibroplasia, reepithelialization, and remodeling. The biologi
cal signals released during the initial clot formation and throughout the r
epair modulate controlled migration, proliferation, and differentiation of
cells actively involved in. this event leading to wound closure. This proce
ss is completed by the synthesis of extracellular matrix proteins in approp
riate quantity and quality. Considerable advances made in understanding cel
l-cell and cell-matrix interactions in cutaneous wound healing provide evid
ence 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 i
s 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-d
epth study. Communication must occur between diverse cell types, many of wh
ich are only transiently present, to recreate a structure that is formed pr
edominantly by cells derived from diverse embryological origin, the epiderm
is from the ectoderm, and the dermis from the mesodermal mesenchyme. This r
eview focuses on the basic mechanisms underlying the interaction of dermal
matrix with surface epithelial layer to facilitate normal wound healing.