I have tried to briefly review the evidence (summarized in Table II) indicating that
fibronectin is important in cutaneous wound healing.
Fibronectin appears to be an important factor throughout this process. It promotes the spreading of platelets at the site of injury, the adhesion and migration of neutrophils, monocytes, fibroblasts, and endothelial cells into the
wound region, and the migration of epidermal cells through the granulation tissue. At the level of matrix synthesis,
fibronectin appears to be involved both in the organization of the granulation tissue and basement membrane. In terms of tissue remodeling,
fibronectin functions as a nonimmune
opsonin for phagocytosis of debris by fibroblasts, keratinocytes, and under some circumstances, macrophages.
Fibronectin also enhances the phagocytosis of immune-opsonized particles by monocytes, but whether this includes phagocytosis of bacteria remains to be determined. In general, phagocytosis of bacteria has not appeared to involve
fibronectin. On the contrary, the presence of
fibronectin in the
wound bed may promote bacterial attachment and
infection. Because of the ease of experimental manipulations, wound healing experiments have been carried out on skin more frequently than other tissues. As a result, the possible role of
fibronectin has not been investigated thoroughly in the repair of internal organs and tissues. Nevertheless, it seems reasonable to speculate that
fibronectin plays a central role in all wound healing situations. Finally, the wound healing problems of patients with severe
factor XIII deficiencies may occur because of their inability to incorporate
fibronectin into
blood clots.