Abstract. Wound contraction can substantially reduce the amount of new tissue needed to reestablish organ integrity after tissue loss. Fibroblasts, rich in F-actin bundles, generate the force of wound contraction. Fibronectin-containing microfibrils link fibroblasts to each other and to collagen bundles and thereby provide transduction cables across the wound for contraction. The temporal relationships of F-actin bundle formation, collagen and fibronectin matrix assembly, and fibronectin receptor expression to wound contraction have not been determined. To establish these relationships, we used a cutaneous gaping wound model in outbred Yorkshire pigs. Granulation tissue filled '~80% of the wound space by day 5 after injury while wound contraction was first apparent at day I0. Neither actin bundles nor fibronectin receptors were observed in 5-d wound fibroblasts. Although fibronectin fibrils were assembled on the surfaces of 5-d fibroblasts, few fibrils coursed between cells. Day-7 fibroblasts stained strongly for nonmuscle-type F-actin bundles consistent with a contractile fibroblast phenotype. These cells expressed fibronectin receptors, were embedded in a fibronectin matrix that appeared to connect fibroblasts to the matrix and to each other, and were coaligned across the wound. Transmission EM confirmed the presence of microfilament bundles, cell-cell and cell-matrix linkages at day 7. Fibroblast coalignment, matrix interconnections, and actin bundles became more pronounced at days 10 and 14 coinciding with tissue contraction. These findings demonstrate that granulation tissue formation, F-actin bundle and fibronectin receptor expression in wound fibroblasts, and fibroblast-matrix linkage precede wound contraction. FIBRONECTIN and actin interrelationships have been of great interest for many years. Early in the study of fibronectin biology, Ali et al. (1977) observed that adding fibronectin to cultures of transformed fibroblasts induced the formation of actin bundles within the cells and concomitantly changed the cells to a more flattened and elongated morphology. In addition, Ali and Hynes (1977) demonstrated that cytochalasin B addition to fibroblast cultures not only caused the disruption of actin filaments but also caused the release of cell surface fibronectin into the medium. An intimate relationship between actin and fibronectin was further established when extracellular fibronectin and intracellular actin were noted to run parallel with each other (Hynes and Destree, 1978). Subsequent transmission electron microscopy studies demonstrated coaxial alignment of intracellular microfilaments and extracellular fibronectincontaining microfilaments across the plasma membrane of hamster and human fibroblasts (Singer, 1979). Furthermore, the reestablishment of this so-called fibronexus was an early event during the fibronectin-induced restoration of normal morphology in transformed fibroblasts (Singer, 1982). More recently, several laboratories (Tamkun et al., 1986; Chen et al., 1985Chen et al., , 1986 Singer...

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The mechanical properties of skin have been studied both in vivo and in vitro by a variety of test methods. These properties are well matched to the function of the skin, and they depend on the geometry of the collagen and elastin networks of the dermis. The time dependence of these properties is thought to be related to the "ground substance" components of the dermis. Age-related changes in the mechanical properties are a function of the degradation of the elastin network and of some as yet undefined changes in the viscoelastic properties of the "ground substance."

Eight stages in the development of the human embryonic and fetal periderm have been established, primarily on the basis of surface morphology, major changes in epidermal stratification, and differentiation. The changes in the periderm observed with the scanning electron microscope have been correlated with and supplemented by cytologic studies with the transmission electron microscope in the periderm and other epidermal layers. Light microscopy was used to determine what proportion of the epidermal thickness is accounted for by the periderm and what relationship individual periderm cells have with underlying cells. The results yield a comprehensive, three-dimensional image of the human epidermis during development and support a concept of the periderm as a layer of "dynamic" cells which project superficial blebs, expand in surface area, then regress at the onset of keratinization, leaving only cellular remnants associated with the adult type epidermis.

A series of linearly incised superficial skin wounds was made on the forearms of young adult male volunteers. Wounds were sampled at several intervals between 3 hr and 21 days after wounding, for study by light and electron microscopy. The light microscopic observations show that regeneration of epidermis in human wounds conforms chronologically to that reported for the epidermis in superficial wound repair in laboratory animals. It is further shown that "ruffling" of cell membranes characterizes the cells of the migrating epidermis in early wound healing. This study reveals that the basement lamina and hemidesmosomes are established by epidermis in contact with the fibrin net at the base of early wounds. Epidermal cells in the wound environment are shown to be phagocytic. Analysis of the submicroscopic cytology of differentiating and maturing regenerated epidermis reveals that, in the sequence of events, the formation of filaments, basal lamina, and desmosomes is followed chronologically by evolution of keratohyalin granules and, subsequently, by keratinization of the surface epidermal elements. The entire sequence of migration, differentiation, and ultimate keratinization in the superficial wounds studied requires 3-5 days for completion.