Keratinocyte-derived growth factors play a role in the formation of hypertrophic scars.
In predisposed individuals, wound healing can lead to hypertrophic scar or keloid formation, characterized by an overabundant extracellular matrix. It has recently been shown that hypertrophic scars are accompanied by abnormal keratinocyte differentiation and proliferation, and significantly increased acanthosis, compared with normal scars. This study addressed the question of whether the development of normal and hypertrophic scars is regulated by differences in the growth factor profiles of both the epidermis and the dermis. The presence of interleukin-1alpha (IL-1alpha), IL-1beta, tumour necrosis factor-alpha (TNF-alpha), platelet-derived growth factor (PDGF), transforming growth factor-beta1 (TGF-beta1), and basic fibroblast growth factor (bFGF) was investigated in biopsies taken from breast reduction scars at 3 and 12 months following surgery. The samples were analysed by immunohistological methods and categorized as scars that remained hypertrophic (HH), became normal (HN) or remained normal after 12 months (NN). The epidermal expression of IL-1alpha was significantly increased in NN scars compared with HN and HH scars 3 and 12 months following operation, whereas the dermal expression showed no difference. PDGF was significantly increased in the dermis of normal scars after 3 months and in both the epidermis and the dermis of hypertrophic scars after 12 months. IL-1beta, TNF-alpha, TGF-beta and bFGF showed no differences. It is hypothesized that impaired production of keratinocyte-derived growth factors, such as IL-1alpha, leads to a decrease in the catabolism of the dermal matrix, whereas augmented epidermal PDGF production leads to increased formation of the dermal matrix in hypertrophic scars. These observations support the possibility that the epidermis is involved in preventing the formation of hypertrophic scars.
Niessen
F B
FB
Department of Plastic, Reconstructive, and Hand Surgery, University Hospital Groningen, Groningen, The Netherlands. ni.essen@wxs.nl
Andriessen
M P
MP
Schalkwijk
J
J
Visser
L
L
Timens
W
W
D000293:Adolescent; D000328:Adult; D017439:Cicatrix, Hypertrophic / Q000378:metabolism* / Q000473:pathology; D004817:Epidermis / Q000033:anatomy & histology / Q000737:chemistry* / Q000473:pathology; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000032:analysis; D006133:Growth Substances / Q000032:analysis*; D006801:Humans; D007150:Immunohistochemistry; D007375:Interleukin-1 / Q000032:analysis; D015603:Keratinocytes / Q000737:chemistry; D008875:Middle Aged; D010982:Platelet-Derived Growth Factor / Q000032:analysis; D018709:Statistics, Nonparametric; D013997:Time Factors; D016212:Transforming Growth Factor beta / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D006133:Growth Substances; D007375:Interleukin-1; D010982:Platelet-Derived Growth Factor; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D016222:Fibroblast Growth Factor 2