Reconstruction of Soft Tissue Defects using Multilayer of Acellular Human Dermal Allograft and Terudermis

Classically autologous split-thickness skin graft or flap surgery has been applied to the case of full-thickness skin defects. However, simple skin graft causes postoperative adhesion and scar contracture, and flap surgery could cause functional and aesthetic trouble due to the scar at the donor site. It is well known that the thicker dermis is transplanted, the lesser adhesion and contracture can be resulted. In spite of all advantages, this thicker layer of dermis can also cause pain, infection, hypertrophic scar and delayed healing at the donor site. Two treatments have been developed and applied to solve the problems mentioned above: one is acellular dermal matrix(Alloderm(R)) and the other is Terumo(R) as a silicon coated artificial dermis on the complex of fiberized collagen from calf skin and athecollagen. In the conventional treatment, skin graft is executed when one layer of Terumo(R) or Alloderm(R) is covered and its survival is sure. This method, however, showed certain limits in the appliance: delayed healing time, longer period of hospitalization and limits of dermis supplying, etc. We have applied multi-layer coverage of these materials with simultaneous or delayed skin graft to shorten healing time and to achieve a better effect of dermis. Among those who need flap surgery because of soft tissue defect, or when severe depression or scar contracture can be expected after surgery, a total of 13 cases have been studied: 7 multilayer Alloderm(R) graft with simultaneous thin split-thickness skin graft, and 6 multilayerTerumo(R) graft with delayed skin graft. In all cases, transplants were successful without any difficulties in healing process: no delayed healing time, no functional deficit as contracture, no contour deformity as depression or hypertrophy.

The effect of the application of growth factors on wound contraction : An experimental study in a fibroblast-populated collagen lattice

Many investigators have reported that collagen gel contraction reflects the mechanism of wound contraction. In 1995, Tsai et al. reported that hypertrophic scar-derived fibroblasts in a connective tissue model possessed the greatest contraction potency when compared with those of normal skin and normal oral mucosa-derived CTMs. In this study, we studied the effect of collagen gel contraction by growth factors such as epidermal growth factor, platelet-derived growth factor, transforming growth factor-bata1, and transforming growth factor-bata3, Skin fibroblasts used in this study were obtained from the explant of rat skin culture. Fibroblasts were cultured in Dulbecco's modified Eagle's medium containing 10% fetal bovine serum. Growth factors were added per FPCL in the desired concentrations and we measured the collagen gel diameters in growth factor-treated FPCL on day 1,2,3, and 4 respectively after starting incubation. We examined the effects of EGF, PDGF, TGF-bata1, TGF-bata3 and the effects of combinations of TGF-bata1 + EGF, TGF-bata1 + PDGF, and TGF-bata1 + TGF-bata3 to contract a collagen gel. EGF has little influence on collagen gel contraction. TGF-bata1 and TGF-bata3 increase the collagen contraction. TGF-bata1 enhanced the contractility of collagen gel according to the concentrations. While TGF-bata3 alone had stimulatory contraction effects at low dose, high doses of TGF-bata3 decreased the potency of collagen gel contraction. A combination of TGF-bata1 and EGF minimally decrease TGF-bata1 activity. A combination of TGF-bata1and PDGF had an effect similar to TGF-bata1 activity. A combination of TGF-bata1 and TGF-bata3 decreased TGF-bata1 activity. According to reports that FPCL contraction is equivalent to the process of wound contraction, growth factors which enhance gel contraction may be related to wound contraction and wound healing. TGF-bata1 is reported to enhance scar formation in fetal wound. EGF accelerates wound healing and inhibits the promotion of hypertrophic scar formation. Compared to the effect of collagen gel contraction in this study, the combination of TGF-bata1 and TGF-bata3 that inhibited the promotion of collagen gel contraction are thought to diminish the formation of scar tissue. As well, EGF that has not enhanced collagen gel contraction is thought to diminish the production of scar tissue. We will study the interactive effects of TGF-bata3, EGF and TGF-bata1 on the contraction of collagen gels in the future.