Growth factors known to have a role in the early phases of wound repair have been applied topically to excisional wounds of experimental animals and patients in order to accelerate their healing (reviewed by Fu et al., 2005). Recombinant human EGF and FGF-2 (rhEGF, rhFGF-2) were reported to accelerate the healing of burn wounds in human patients by 1-4 days (Brown et al., 1989; Fu et al., 1998). TGF-p and human growth factor (hGF) were reported to accelerate normal wound repair in both young and old rats (Puolakkainen et al., 1995; Roberts, 1995). Topical application of TGF-P increased the rate of re-epithelialization and contraction in rat and pig incisional wounds and in guinea pig and pig punch wounds (Franzen et al., 1995). Collagen synthesis was increased, leading to increased strength of scar tissue (Roberts, 1995). Intravenous delivery of 100-500 |g/kg of TGF-P to old rats prior to wounding or 4 hr after wounding increased the tensile strength of scar tissue to the level seen in the untreated wounds of young rats. This effect was considerably diminished if the TGF-P was delivered 48 hr after wounding, suggesting that the beneficial effect of the growth factor is through the attraction of neutrophils, macrophages, and fibroblasts early in the repair process. Estrogen levels affect the levels of TGF-P in females and thus wound repair (Ashcroft et al., 1997). Older women have reduced rates of healing and lower levels of scarring, both of which are associated with reduced levels of TGF-P and are reversed by hormone replacement therapy. Ovariectomized young female rats exhibit delayed wound repair that is reversed by estrogen administration, which results in an increase of TGF-P secretion by dermal fibroblasts.
Recombinant human growth hormone (rhGH) has also been shown to increase the mechanical strength of granulation tissue in incisional skin wounds of rats up to 94% that of unwounded skin (Jorgensen and Oxlund, 1996). The increase was dose-dependent and was associated with a nearly 150% increase in the deposition rate of collagen in the wound. Local application of rhGH in subcutaneous wound chambers, or systemic administration of the hormone, stimulated the formation of granulation tissue (Steenfos and Jansson, 1992). Human growth hormone was reported to accelerate healing of donor skin sites in burned children (Herndon et al., 1990; Gilpin et al., 1994). The effects of rhGH
may be both local and systemic. Growth hormone stimulates the production of IGF-I by the liver, elevating the serum level of IGF-I, which as a cell cycle competence factor would then stimulate fibroblast proliferation (Jorgensen and Oxlund, 1996). rhGF may also have a direct effect on fibroblast proliferation, since receptors for the hormone are present in skin fibroblasts (Lobie et al., 1990).
Some studies have obtained less positive results (reviewed by Greenalgh, 1996). FGF-2 was reported to have no effect on the rate of re-epithelialization, wound closure, or scarring at donor sites of partial-thickness skin grafts in burned children (Greenalgh and Rieman, 1994) and Cohen et al. (1995) found no effect of EGF on the rate of epithelial closure. On balance, the evidence would suggest that TGF-P, FGF-2, HGF, EGF, GH, and IGF-I are able to accelerate the repair of acute wounds in normal skin (Fu et al., 2005).
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