Inhibitory effects of local pretreated epidermis on wound scarring: A feasible method to minimize surgical scars
Introduction
Each year in the developed world, 100 million patients acquire scars as a result of 55 million elective operations and 25 million operations after trauma [1]. Scars arise after almost every deep dermal injury. Scars are regarded as the outcome of prolonged inflammation, which causes excessive proliferation of fibroblasts (FBs) and overproduction of collagen. Bleeding, infection of the wound and tension across the incision edges are the major factors concerned with scarring [2]. No injury, no scarring. A prolonged lack of skin integrity is the primary factor inducing scarring. If only the epidermis is damaged, the wound will be re-epithelized in 2 weeks and heal without scarring. If the cutaneous trauma is so severe that the skin integrity cannot be restored until the 3rd–4th week post-trauma, raised scars are a potential outcome. In normal dermis, there is a balance between the proliferation and degradation of FBs. After the skin is severely damaged, FBs around the wound begins to proliferate and synthesize collagen, forming granulation tissue before re-epithelization takes place [2]. When a wound heals spontaneously, the granulation tissue is usually replaced by hypertrophic scar, which generally regresses spontaneously, becoming pale and flat, several months later when the epidermal structure of scar is approximately similar to that of normal skin. In addition, wound scarring can be minimized by skin grafting, or by grafting of epidermis [3]. All these clinical findings imply that epidermis might modulate the bioactivity of FBs and the long-time absence of epidermis can be one of the chief causes of scarring. This hypothesis has been confirmed by many relevant experimental and clinical studies. Cultured epithelial autografts (CEA) have been utilized in the treatment of burn patients for decades. Clinical experience showed CEA could close the full-thickness burn wounds with decreased hypertrophic scar formation [3]. In vitro the proliferation abilities of the suprapapillary FBs are significantly diminished as compared to papillary FBs, partly because epidermis can release epidermal derived factors (EDF) and epidermal chalone (growth inhibitory epidermal pentapeptide), both inhibitors of fibroblast growth [4], [5], [6]. The epidermis of hypertrophic scar has less cell layers and cellular organs than that of normal skin, which may down-regulate the inhibitors (EDF and epidermal chalone) synthesis and impair the contact inhibition of epidermis on FBs activity [7]. But epidermis or keratinocytes of pathological scars excrete or express more vascular endothelial growth factor (VEGF), transforming growth factor (TGF) and Langerhans cells, which are among molecular or cellular factors playing an important part in scar formation [8].
For these readings, maintaining a normal epidermis on a dermal wound may be a feasible method to prevent scarring. In an effort to test this hypothesis clinically, the present study was designed to assess the healing of surgical incision or skin grafting recipient area performed by a new surgical skill involved epidermis management.
Section snippets
Reagents
For immunohistochemistry, SABC universal kit, rabbit anti-human polyclonal anti-type collagen and anti-type III antibody and Biotinylated goat anti-rabbit immunoglobulin G was provided by Boster Biological Technology Ltd. (Wuhan, PR China). Haematoxylin–eosin and 3,3′-diaminobenzidine used as chromogen were obtained from Sigma Chemical Co. (St. Louis, MO, USA).
Patient selection
All subjects were recruited at the Surgical Division of the Nanfang Hospital (Guangzhou, PR China). Eight patients (Population 1) were
Clinical examination
In Population 1, sutures of the wounds were removed at seven days after operation and all wounds healed perfectly without any infection or necrosis. The control group had been found to scar since the second postoperative week, when the subjective itching sensation reached its peak. The scars of five incisions in the control group became progressively larger and remained pigmented during the whole study period. In the experimental group, the repositioned epidermis integrated to the surrounding
Discussion
Scars are the end point of the normal continuum of mammalian tissue repair. The ideal end point would be total regeneration, with the new tissue having the same structural, aesthetic, and functional attributes as the original uninjured skin. However, scarring may be an inevitable sequel to full-thickness cutaneous injury, such as surgical incision [1]. Some surgical skills, such as incising skin along Langer's lines, intradermally suturing and skin grafting, will improve cutaneous repair for
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