A surgical approach for earlobe keloid: keloid fillet flap

Earlobe keloid can form after cosmetic ear piercing, trauma, or burns, and it poses several difficulties in treatment and distinctive cosmetic implications. Treatment methods for earlobe keloids include both surgical and nonsurgical methods. After excision of the earlobe keloid, healing by secondary intention, primary suture, skin graft, or local flap has revealed some disadvantages. The authors approached this problem with a new excision and covering method. The surgery was performed under local anesthesia. Skin over the keloid was dissected from the keloid mass as a flap, which they termed a "keloid fillet flap," and the keloid mass was completely removed. Subcutaneous sutures were not used, and the keloid fillet flaps were closed with 6-0 nylon sutures after trimming. Other intraoperative or postoperative preventive procedures, such as steroid injection, pressure device, or irradiation, were not applied primarily. In the period from May of 1999 to October of 2000, nine earlobe keloids in eight patients were treated with this protocol. One patient had bilateral keloids. Of the eight patients, there were six women and two men, ranging in age from 21 to 61 years (mean age, 28.5 years). The causes of keloids were ear piercing in six cases and trauma in three cases. The largest lesion was 3 cm in its greatest dimension, and the smallest was 1.5 cm (mean, 2.3 cm). All flaps survived completely. There were four cases of recurrence. Seven cases, including two recurrences, showed good results. The authors believe the recurrence of earlobe keloid was closely related to the method for coverage of the defect after its surgical excision, and the "5 As and one B" (Asepsis, Atraumatic technique, Absence of raw surface, Avoidance of tension, Accurate approximation of wound margin, and complete Bleeding control) are important factors in reducing the recurrence rate of earlobe keloids in surgical excision. The authors' protocol is very effective in closing the defect after surgical excision of earlobe keloids and offers many advantages over other surgical approaches. The recurrence rate of earlobe keloid may be lower than in their results if other intraoperative and postoperative treatment procedures are combined with their protocol.     

Tissue alpha-globulins in keloid formation.

The deposition of alpha-1-antitrypsin and alpha-2-macroglobulin, both known to be inhibitors of human skin collagenase, is significantly increased in keloids and in hypertrophic scars (as compared to normal skin). However, following intralesional triamcinolone treatment, a marked resorption of these abnormal scars occurs along with a significant reduction of the alpha-1-antitrypsin deposits. These findings suggest that alpha-globulins are involved in abnormal scar formation, and that triamcinolone may remove collagenase and/or protease inhibitors--thereby allowing activation of the collagenase with subsequent breakdown and resorption of the excessive collagen.     

The role of the activin system in keloid pathogenesis

Keloid scars represent a pathological response to cutaneous injury under the regulation of many growth factors. Activin-A, a dimeric protein and a member of the transforming growth factor- superfamily, has been shown to regulate various aspects of cell growth and differentiation in the repair of the skin mesenchyme and the epidermis. Thus our aim was to study the role of activin and its antagonist, follistatin, in keloid pathogenesis. Increased mRNA expression for activin was observed in keloid scar tissue by performing RNase protection assay. Immunohistochemistry showed increased localization of both activin-A and follistatin in the basal layer of epidermis of keloid tissue compared with normal tissue. ELISA demonstrated a 29-fold increase in concentration of activin-A and an 5-fold increase in follistatin in conditioned media in keloid fibroblasts compared with normal fibroblasts. Although keloid keratinocytes produced 25% more follistatin than normal keratinocytes, the amounts of activin-A, in contrast, was 77% lower. Proliferation of fibroblasts was stimulated when treated with exogenous activin-A (46% increase in keloids fibroblasts) or following co-culture with hAHaCaT cells (66% increase). Activin-A upregulated key extracellular matrix components, namely collagen, fibronectin, and -smooth muscle actin, in normal and keloid fibroblasts. Co-treatment of follistatin with activin-A blocked the stimulatory effects of activin on extracellular matrix components. These findings emphasize the importance of the activin system in keloid biology and pathogenesis and suggest a possible therapeutic potential of follistatin in the prevention and treatment of keloids. collagen; fibroblasts; follistatin; keloid scar; keratinocytes; -smooth muscle actin; transforming growth factor-     

From genetics to epigenetics: new insights into keloid scarring

Keloid scarring is a dermal fibroproliferative response characterized by excessive and progressive deposition of collagen; aetiology and molecular pathology underlying keloid formation and progression remain unclear. Genetic predisposition is important in the pathogenic processes of keloid formation, however, environmental factors and epigenetic mechanisms may also play pivotal roles. Epigenetic modification is a recent area of investigation in understanding the molecular pathogenesis of keloid scarring and there is increasing evidence that epigenetic changes may play a role in induction and persistent activation of fibroblasts in keloid scars. Here we have reviewed three epigenetic mechanisms: DNA methylation, histone modification and the role of non‐coding RNAs. We also review the evidence that these mechanisms may play a role in keloid formation ‐ in future, it may be possible that epigenetic markers may be used instead of prognostic or diagnostic markers here. However, there is a significant amount of work required to increase our current understanding of the role of epigenetic modification in keloid disease.