The pathogenesis of keloid remains poorly understood. As no effective therapy for keloid is as yet available, an insight into its pathogenesis may lead to novel approaches. Apoptosis has been found to mediate the decrease in cellularity during the transition between granulation tissue and scar. Here, we report that in contrast to hypertrophic scar-derived and normal skin-derived fibroblasts, keloid-derived fibroblasts are significantly resistant to both Fas-mediated and staurosporine-induced apoptosis. The caspases-3, -8, and -9 were not activated indicating that the block in the apoptotic pathway in keloid is upstream of the caspases. There were no significant differences in the level of expression of Fas, Bcl-2, and Bax between the three groups but addition of transforming growth factor (TGF)-beta1 significantly inhibited Fas-mediated apoptosis in hypertrophic scar-derived and normal skin-derived fibroblasts and neutralization of autocrine TGF-beta1 with anti-TGF-beta1 antibody abrogated the resistance of keloid-derived fibroblasts. Anti-apoptotic activity was not observed with TGF-beta2. This is the first study linking refractory Fas-mediated apoptosis to cellular phenotype in keloids and indicating a pivotal role for the anti-apoptotic effect of TGF-beta1 in this resistance. Hence, it becomes important to treat keloids as a separate entity different from hypertrophic scars and enhancement of Fas-sensitivity could be a promising therapeutic target.
We studied the long-term outcome of injection of triamcinolone acetonide into keloid scars in Asian patients. Between 1985 and 2003, we treated 109 keloid scars in 94 patients by injecting 1 to 10?mg of triamcinolone acetonide depending on the size of the lesion at four week intervals. There was little morbidity. Thirty-one patients gave up treatment within 10 injections because of pain and lack of immediate improvement. Improvement in subjective symptoms was seen in 52 of the remaining 63 patients (82%). In objective symptoms, fair or better results were seen in 40 of 63 (63%), and good or better results in 25 of 63 (39%). The treatment method required 20-30 injections over three to five years. Although we did not achieve as good results as other authors, we think it was safer because we used a smaller dose of a steroid.
Basic fibroblast growth factor (bFGF) is well known to promote the proliferation of almost all cells associated with wound healing. However, as the activation duration of bFGF is very short in vivo, we incorporated bFGF into an acidic gelatin hydrogel and studied the sustained release of bFGF in vivo. In addition, we investigated the effects of the acidic gelatin sheet containing bFGF on wound healing. To distinguish wound contraction from neoepithelialization, we measured both the wound area and neoepithelium length. Other histological parameters such as thickness of granulation tissue and number of capillaries were also determined as indices of wound healing. Fibrous tissue was assessed using an Elastica van Gieson and Azan stain. A skin defect (1.5 x 1.5 cm) of full thickness was created on the back of each test mouse and the wound was covered with an acidic gelatin hydrogel, referred to as a gelatin sheet in this study (2 x 2 cm), with bFGF (100 microg/site) (A) or without bFGF (B). 1, 2, 3, 5, 7 and 14 days after covering, mice were killed and an enzyme-linked immunosorbent assay (ELISA) was performed to estimate the concentration of bFGF in the plasma. In another experiment, each wound was covered with (A), (B) or a hydrogel dressing (control group, C) and the wound area was measured 1 or 2 weeks postoperatively with a computer planimeter. The histological parameters, as mentioned above, were assessed using a light microscope. Sustained release of bFGF from the gelatin sheet was observed and the gelatin sheet containing bFGF promoted neoepithelialization, granulation, neovascularization and wound closure. This gelatin sheet containing bFGF was concluded to be effective for wound healing and promising for clinical use.
A major disadvantage of free radial forearm flaps is the conspicuous donor site. However, there have been few studies on donor scars. The authors evaluated the donor site in patients who underwent oral-floor reconstruction with a free radial forearm flap. The subjects were 23 patients (19 males and four females) who underwent reconstruction with a free radial forearm flap following resection of a malignant oral tumor, and were followed for 1 year or longer. The fasciocutaneous flap collection site was closed by full-thickness skin graft (FTSG) from the groin with tie-over dressing. All grafts took perfectly. At the scar at the donor site, five items (pigmentation, scar width, depression, wrist mobility, and sensory abnormalities) were evaluated. Depression and pigmentation were often observed, but patient dissatisfaction was slight. While their main postoperative concern was the oral reconstruction site, after about 1 year, the donor site became more important to patients. However, the results were good. A 100 percent take of the FTSG at the donor site should produce good results. Surgeons should pay adequate attention not only to the outcome at the reconstruction site, but also to the closure of the donor site.
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