Wide spread scars, hypertrophic scars, and keloids

Patients with a wide scar may complain of having a "keloid," yet have a hypertrophic or a wide spread scar. The plastic surgeon should make the appropriate clinical diagnosis, because therapy varies depending on the condition present. A wide spread scar is best treated with excision and closure. A buried dermal flap may help to prevent recurrence, which is nevertheless likely to some degree. A hypertrophic scar can be distinguished from a keloid on clinical grounds. Although both may be red, nodular, and itchy, the keloid overgrows the original wound boundary and is much more likely to recur after surgical excision. Nonsurgical treatment of hypertrophic scars and keloids is similar, using repeated intralesional injections of Kenalog 40 mg per cc and sustained pressure on the lesion when possible. Surgical treatment differs for hypertrophic scars or keloids. Scar excision and closure, and selective Z-plasty, may be used in hypertrophic scars. In keloids, aggressive surgery is usually avoided, unless the lesion has a narrow pedicle. Surgery of keloids should be accompanied by intra- and postoperative Kenalog-40 injections, and on occasion by sustained pressure. Very large keloids may be resistant to medical management, and too aggressive for surgery owing to a high likelihood of recurrence. These difficult lesions serve as the impetus for continued biochemical and tissue culture research, seeking a biochemical means of control keloids.     

Tenascin-C在瘢痕疙瘩和增生性瘢痕中的基因表达研究

目的 探讨Tenascin-C基因在瘢痕疙瘩和增生性瘢痕中的表达。方法 取正常成人皮肤组织RNA，构建正义、反义Tenascin-C(Tn-C)mRNA探针，运用原位杂交技术，观测10例瘢痕疙瘩、10例增生性瘢痕和5例正常成人皮肤组织中Tn-C mRNA的表达。结果 Tn-C mRNA在正常皮肤表皮中无表达，真皮中表达稀少，局限于乳头真皮层的成纤维细胞和皮肤附属器；10例瘢痕疙瘩表皮均有表达，真皮分布较广，如成纤维细胞、血管内皮和皮肤附属器；Tn-C mRNA在3例增生性瘢痕表皮表达，7例无表达，真皮中表达与瘢痕疙瘩相同但较弱，比正常皮肤增多，但差异无显著性。结论 Tenascin-C mRNA在瘢痕疙瘩表皮和真皮中有高表达。     

Study of microvascular structure in keloid and hypertrophic scars: density of microvessels and the efficacy of three-dimensional vascular imaging

We have investigated the blood vessels in keloids and hypertrophic scars, both morphologically and statistically. We also tried to construct three-dimensional images of blood vessels in a keloid and hypertrophic scar to clarify the vascular patterns. Keloids (n = 16) and hypertrophic scars (n = 12) were stained with haematoxylin and eosin, and immunostained with anti-CD31 antibody. The capillary density (number/1.0 mm(2)) and length of the major and minor axes were measured, and the major:minor axis ratio was calculated. Eighty serial sections were prepared from the preparations. Using image preparation software (Realia, INTAGE), the 80 input images were superimposed to construct a three-dimensional image of blood vessels in the tissue. We initially succeeded in constructing three-dimensional images of blood vessels in a keloid and hypertrophic scar. By statistical analysis of the vascular density and morphology, we clarified that there were fewer capillaries in keloids than in hypertrophic scars (p < 0.01), and that the vascular lumen was flattened. Capillaries in the central region of keloids tended to flat, compared with those in the marginal region. Three-dimensional images suggested that there was no microvascular communication in keloids; there was also an inadequate blood supply in keloid tissue. These findings may be a result of the growth of collagen and fibroblasts with keloid maturation.     

Activated caspase expression and apoptosis increase in keloids: cytochrome c release and caspase-9 activation during the apoptosis of keloid fibroblast lines

To characterize apoptosis in keloids and the mechanisms responsible for this process, the expression of activated caspase-9 and -3 in fibroblasts obtained from keloids was analyzed. Immunohistochemistry revealed that the number of fibroblasts positive for terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL) or activated caspase-9 or -3 was low but was significantly higher in keloid tissues than in normal scar tissues. Significant relationships between the number of caspase-positive fibroblasts and TUNEL-positive fibroblasts suggested that the activation of caspase-9 and -3 induces apoptosis in a subpopulation of keloid fibroblasts. All keloid fibroblast cell lines established in this study showed activation of caspase-9 and -3 after serum deprivation for 3 or 4 hours, as shown using Western blotting. Furthermore, serum deprivation-induced apoptosis in a keloid fibroblast line was blocked by a caspase-9 inhibitor (acetyl-Leu-Glu-His-Asp-al), indicating that activation of caspase-9 was necessary for the process of apoptosis in keloid fibroblasts. Although serum deprivation did not significantly change the level of apoptosis protease activating factor-1 in any of the lines, cytochrome c release was detected in cytosolic fractions of the lines after serum deprivation for 3 or 4 hours. These results strongly suggest that keloid fibroblasts are predisposed to apoptosis and cytochrome c release and that caspase-9 activation may underlie regulation of apoptosis in keloid fibroblasts in vivo.     

Hypertrophic scars and keloids

Excessive scarring caused by pathologically overabundant collagen deposition is a problem known by all surgeons. Complications to wound healing, such as hypertrophic scars and keloids, can lead to an aesthetically unacceptable result or even lead to anatomic dysfunction. An overwhelming amount of hypotheses concerning treatment of these problems is available. There seems to be no absolutely effective treatment for hypertrophic scars and keloids and the number of treatment modalities illustrate the lack of understanding concerning this kind of pathologic scar healing. Most studies reported have not been well controlled and have produced conflicting results.     

性激素受体在瘢痕中的表达及与细胞周期调控蛋白相互关系的研究

目的　了解雄激素受体 (AR)、雌激素受体 (ER)在病理性瘢痕中的表达及其与细胞周期调节蛋白D1(cyclinD1)、p16之间的相互关系 ,以探讨他们在瘢痕形成过程中的作用及机制。方法　采用免疫组化方法 (SP法 )对 30例瘢痕标本进行研究 ,以正常皮肤组织为对照 ,观察上述指标的表达。结果　正常皮肤及普通瘢痕成纤维细胞中所有指标均为阴性 ;增生性瘢痕与瘢痕疙瘩成纤维细胞中cyclinD1、p16、AR与正常皮肤相比差异均有显著性意义 (P <0 0 5 ) ;瘢痕疙瘩成纤维细胞cyclinD1和AR的表达高于增生性瘢痕 ,且有显著性意义 (P <0 0 5 ) ;p16在瘢痕疙瘩成纤维细胞的表达比增生性瘢痕为高 ,但两者之间差异无显著性意义。在病理性瘢痕中cyclinD1和AR的表达具有明显的相关性。结论　AR在病理性瘢痕的发生及发展中起一定的作用 ,它可能是通过与其配体结合后促使与cyclinD1有关的基因表达而发挥作用的。在瘢痕疙瘩里可能存在cyclinD1的促细胞增生作用超过P16细胞抑制 ,所以细胞呈现持续增殖状态 ;而在增生性瘢痕里cyclinD1与p16可能处于相对的平衡状态 ,细胞生长具有一定的自限性。     

Effects of steroids,interferon-2B,or interluekin 1B on apoptosis of fibroblasts from keloid,hypertrophic scars,and normal skin and related signal pathway

Wound healing can lead to hypertrophic scar or keloid formation, characterized by an overabundant extracellular matrix. Current established treatment strategies include surgical resection, triamcinolone steroid injection, pressure therapy, silicone therapy, radiotherapy, etc. Cytokines also play a critical role in the regulation of cellular activities and extracellular matrix metabolism. Interferons (IFN) represent a group of antifibroproliferative agents that inhibit fibroblast proliferation and collagen production, and interleukin (IL)-1β also accelerates hypertrophic scar fibroblasts to produce collagenolytic enzymes, leading to tissue destruction. This study addressed the effects of steroid, IFN α-2b, or IL-1β on apoptosis and cell pathway of fibroblasts from keloids, hypertrophic scars, and normal skins and different responses of different fibroblasts. Six samples of keloid, six samples of hypertrophic scar, and six samples of normal skin were, respectively, collected from patients, and fibroblasts from different sources were cultured in vitro. After different fibroblasts were treated with dexamethasone (0.1 mg/ml) or IFN α-2b (1,000 μ/ml) or IL-1β (200 μ/ml), Bax and Bcl-2 were detected in situ by immunohistochemical staining; deoxyribonucleic acid ladders of different fibroblasts were observed by gel electrophoresis, and relative activated (phospho-) extracellular-signal-regulated kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK) pathways were detected by the method of fast activated cell-based enzyme-linked immunosorbent assay. In media containing dexamethasone, apoptosis took place in fibroblasts from keloids, hypertrophic scars, and normal skins by gel electrophoresis with increased rate of Bax/Bcl-2. Activated (phospho-) ERK1/2 and activated (phospho-) JNK expressions increased in three different fibroblasts. In media containing IFN α-2b, no apoptosis took place in three different fibroblasts without any change of expressions of Bax and Bcl-2 except for the expression of decreased Bcl-2 in fibroblasts from keloids. Activated (phospho-) ERK1/2 expression decreased in fibroblasts from keloid and hypertrophic scars without any changes of activated (phospho-) JNK expression, and IFN α-2b did not affect both activated (phospho-) ERK1/2 and activated (phospho-) JNK expressions in fibroblasts from normal skin. In media containing IL-1β, apoptosis of fibroblasts from keloids was induced by stimulating activated (phospho-) ERK1/2 and activated (phospho-) JNK pathways; IL-1β could not induce apoptosis of fibroblasts from normal skin (radio of Bax/Bcl-2 decreasing) whose activated (phospho-) ERK1/2 pathway was stimulated without any changes of activated (phospho-) JNK expression. Apoptosis in fibroblasts from hypertrophic scars was induced by activating the JNK pathway and prohibiting the ERK1/2 pathway. The effects of steroid, IFN α-2b, or IL-1β on apoptosis of different fibroblasts were different through different cell signal pathways, although all of them were effective for treatment of abnormal scars.     

Study of microvascular structure in keloid and hypertrophic scars: Density of microvessels and the efficacy of three-dimensional vascular imaging

Abstract

We have investigated the blood vessels in keloids and hypertrophic scars, both morphologically and statistically. We also tried to construct three-dimensional images of blood vessels in a keloid and hypertrophic scar to clarify the vascular patterns. Keloids (n = 16) and hypertrophic scars (n = 12) were stained with haematoxylin and eosin, and immunostained with anti-CD31 antibody. The capillary density (number/1.0 mm²) and length of the major and minor axes were measured, and the major:minor axis ratio was calculated. Eighty serial sections were prepared from the preparations. Using image preparation software (Realia, INTAGE), the 80 input images were superimposed to construct a three-dimensional image of blood vessels in the tissue. We initially succeeded in constructing three-dimensional images of blood vessels in a keloid and hypertrophic scar. By statistical analysis of the vascular density and morphology, we clarified that there were fewer capillaries in keloids than in hypertrophic scars (p < 0.01), and that the vascular lumen was flattened. Capillaries in the central region of keloids tended to flat, compared with those in the marginal region. Three-dimensional images suggested that there was no microvascular communication in keloids; there was also an inadequate blood supply in keloid tissue. These findings may be a result of the growth of collagen and fibroblasts with keloid maturation.     

异常瘢痕成纤维细胞在低血清及白介素1β作用下的细胞凋亡研究

目的 明确低血清及白介素1β（IL-1β）对瘢痕疙瘩,增生性瘢痕及正常皮肤成纤维细胞诱导细胞凋亡的作用。方法 对6例瘢痕疙瘩、6例增生性瘢痕及6例正常皮肤标本采用细胞培养、免疫组织化学及凝胶电泳方法,通过检测Bax,Bcl-2蛋白及特异性DNA梯形条带,对不同成纤维细胞在低血清中及IL-1β作用后的细胞凋亡进行了研究。结果 （1）在低血清中,瘢痕疙瘩和增生性瘢痕成纤维细胞的Gax/Bcl-2蛋白表达比值没有明显改变,但增生性瘢痕成纤维细胞出现程度较轻的细胞凋亡,而瘢痕疙瘩成纤维细胞未见明显细胞凋亡;正常皮肤成纤维细胞出现细胞凋亡,且Bax/Bcl-2比值升高,表明发生细胞凋亡,（2）IL-1β作用下,三者成纤维细胞均发生凋亡,瘢痕疙瘩和增生性瘢痕凋亡比正常皮肤严重。但Bax/Bcl-2比值在瘢痕疙瘩升高,在正常皮肤降低。增生性瘢痕无明显变化。结论 不同的成纤维细胞特性存在差异。     

Gelatinase activity in keloids and hypertrophic scars

Keloids and hypertrophic scars are characterized by excessive deposition of collagen, which may result from insufficient protein degradation. Little is known about the levels of two gelatinases, matrix metalloproteinase-2 (72 kD type IV collagenase) and matrix metalloproteinase-9 (matrix metalloproteinase-9; 92 kD type IV collagenase) in these abnormal scars. The purpose of this study was to determine levels of these proteinases in tissue from hypertrophic scars, keloids, and donor skin. Ten hypertrophic scar samples, 9 keloid samples, and 10 donor skin samples were frozen, pulverized, homogenized, clarified by centrifugation, and analyzed for matrix metalloproteinases by quantitative zymography. Identity of matrix metalloproteinases was determined using a conditioned media reference standard, molecular weight ladders, and Western blotting. Levels of matrix metalloproteinase-9 activity were very low or undetectable in all samples. However, matrix metalloproteinase-2 activity was significantly elevated in keloids and hypertrophic scars vs. donor samples: 2.6 and 3.9-fold increases for latent matrix metalloproteinase-2, 7.8 and 6.9-fold increases for active matrix metalloproteinase-2, respectively. We conclude that little matrix metalloproteinase-9 activity (the gelatinase involved in early tissue repair) is present in keloids and hypertrophic scars, while matrix metalloproteinase-2 activity (the gelatinase involved in prolonged tissue remodeling) is present in donor skin and is significantly increased in hypertrophic scars and keloids.     

病理性瘢痕中c-myc、c-fos和ras原癌基因表达的实验研究

目的 探讨原癌基因的表达与病理性瘢痕形成的相关性。方法 应用免疫组化SP法及图像定量分析，检测c-myc、c-fos和ras p21蛋白在增生性瘢痕、瘢痕疙瘩和正常皮肤组织中的表达，结果 在增生性瘢痕和瘢痕疙瘩的成纤维细胞中c-myc和c-fos呈强阳性表达，而ras p21蛋白在病理性瘢痕的成纤维细胞中缺乏表达。结论 ①病理性瘢痕中c-myc和c-fos癌基因受激活，可能参与了成纤维细胞的分化增殖、胶原合成与降解以及对细胞因子的调控，并导致瘢痕增生。②ras癌基因在病理性瘢痕形成中可能不突变或不起主要作用。③病理性瘢痕只是部分原癌基因的有限制性表达，不存在多基因无限制性的共同表达可能是其较少癌变的原因。     

Hydration and occlusion treatment for hypertrophic scars and keloids.

In 31 patients with hypertrophic scars or keloids, a side by side test was carried out to check the efficacy of an occlusive dressing technique using cream which did not contain silicone oil, versus a simple application of vaseline, used as a control. In all cases, the cream treated areas of scar and keloid demonstrated a remarkable improvement over that of the vaseline treated area. These findings strongly suggest that the mechanisms of hydration and occlusion are the main basis of the therapeutic action of this method in treating hypertrophic scars and keloids.     

整合素α5β1在病理性瘢痕中的表达及意义

目的　研究整合素α5β1 在病理性瘢痕中的表达情况 ,探讨其在瘢痕发生、发展中的作用和意义。方法　运用SP免疫组化及SPA 胶体金免疫电镜技术对 15例增生性瘢痕、15例瘢痕疙瘩及 10例正常皮肤进行整合素α5β1 的检测 ,并对结果进行半定量及定量分析。结果　在瘢痕疙瘩和增生性瘢痕的成纤维细胞中整合素α5β1 呈阳性表达 ,较正常皮肤强 (P <0 0 1) ;在瘢痕疙瘩中的表达较增生性瘢痕强 (P <0 0 1)。结论　整合素α5β1 与病理性瘢痕发生、发展关系密切。设法减少整合素α5β1 在成纤维细胞的过度表达或许是抑制瘢痕增生、软化瘢痕的新途径     

病理性瘢痕中c-fos原癌基因的表达

目的　病理性瘢痕是创伤过度愈合的结果 ,以成纤维细胞的异常增殖、合成及分泌大量胶原和细胞外基质为特征 ,其形成机理仍不清楚。探讨原癌基因c -fos的表达与病理性瘢痕形成的相关性。方法　应用免疫组化SP法 ,检测c -fos蛋白在增生性瘢痕、瘢痕疙瘩及正常皮肤组织中的表达和分布 ,并用图像定量分析比较其差异。结果　在增生性瘢痕和瘢痕疙瘩的成纤维细胞中c-fos呈强阳性表达 ,两组间无明显差异 ,而与正常皮肤对照组均有显著性差异。结论　增生性瘢痕与瘢痕疙瘩中c -fos蛋白表达升高 ,存在c -fos癌基因的激活 ,可能参与了成纤维细胞的分化增殖、胶原合成与降解以及对细胞因子的调控 ,并导致瘢痕增生     

病理性瘢痕中c-fos原癌基因的表达

目的　病理性瘢痕是创伤过度愈合的结果,以成纤维细胞的异常增殖、合成及分泌大量胶原和细胞外基质为特征,其形成机理仍不清楚。探讨原癌基因c-fos的表达与病理性瘢痕形成的相关性。方法　应用免疫组化SP法,检测c-fos蛋白在增生性瘢痕、瘢痕疙瘩及正常皮肤组织中的表达和分布,并用图像定量分析比较其差异。结果　在增生性瘢痕和瘢痕疙瘩的成纤维细胞中c-fos呈强阳性表达,两组间无明显差异,而与正常皮肤对照组均有显著性差异。结论　增生性瘢痕与瘢痕疙瘩中c-fos蛋白表达升高,存在c-fos癌基因的激活,可能参与了成纤维细胞的分化增殖、胶原合成与降解以及对细胞因子的调控,并导致瘢痕增生。     

病理性瘢痕中原癌基因c-myc和c-fos的表达

目的　探讨原癌基因的表达与病理性瘢痕形成的相关性。方法　应用免疫组化SP法 ,检测c -myc和c -fos蛋白在增生性瘢痕、瘢痕疙瘩和正常皮肤组织中的表达和分布 ,并用图像定量分析比较其差异。结果　在增生性瘢痕和瘢痕疙瘩的成纤维细胞中c-myc、c -fos呈强阳性表达 ,两组间无明显差异 ,而与正常皮肤对照组均有显著性差异。结论　增生性瘢痕与瘢痕疙瘩中c -myc、c -fos蛋白表达升高 ,存在c -myc和c -fos原癌基因的激活 ,可能参与了成纤维细胞的分化增殖或表型转化、胶原合成与降解以及对细胞因子的调控 ,并导致瘢痕增生。     

p53 and apoptosis alterations in keloids and keloid fibroblasts

Keloids are the result of a dysregulated wound-healing process and are characterized by formation of excess scar tissue that proliferates beyond the boundaries of the inciting wound. In this study, we investigated the expression of key proteins involved in regulating apoptosis in keloids. Twenty archival paraffin-embedded keloid samples were randomly selected for an immunoperoxidase assay with antibodies against fas, p53, bcl-2, and bcl-x proteins using the target antigen-retrieval technique. Apoptosis was assessed in keloids and normal skin and in keloid and normal fibroblasts by the TdT-mediated dUTP nick-end labeling (tunel) assay on tissue sections, fibroblast cultures, and by flow cytometry for cell suspensions. We found that 18 of 20 keloids expressed p53 protein; bcl-2 was expressed by keloid fibroblasts in 19 of 20 keloids, and all specimens had prominent fas expression throughout the tissue. The distribution of these three antigens was regional within each lesion and followed a consistent pattern of p53 and bcl-2 expression colocalized to the hypercellular, peripheral areas of each keloid in a perinuclear pattern (p < .001). In contrast, an inverse distribution of fas expression was shown, with staining being more diffuse across the cell surfaces and limited to the central, more hypocellular regions in 16 of 17 keloids (p < .001). There was no specific staining pattern in these keloids with antihuman bcl-x. In vitro studies on cultured keloid fibroblasts (derived from six patients) revealed maintenance of the p53+, bcl-2+ phenotype up to passage 10. Neither neonatal nor normal adult skin fibroblasts expressed either antigen but could be induced to express p53 by exposure to adriamycin. Keloid lesions and keloid fibroblasts were found to have lower rates of apoptosis than normal controls. Keloid fibroblasts displayed enhanced apoptosis rates in response to hydrocortisone, γ interferon and hypoxia treatment as compared with normal adult fibroblasts. Focal dysregulation of p53 combined with upregulation of bcl-2 may help produce a combination of increased cell proliferation and decreased cell death in the younger hypercellular areas of the keloid. This phenotype is reversed in the older areas of the keloid and may prevent malignan degeneration, thus favoring normal apoptosis as evidenced by prominent fas expression.     

Postoperative radiation protocol for keloids and hypertrophic scars: statistical analysis of 370 sites followed for over 18 months

BACKGROUND: Before 2002, keloids and intractable hypertrophic scars were treated at our facility with postoperative irradiation of 15 Gy (the traditional protocol). Analysis of the therapeutic outcomes of patients treated with this protocol showed that the recurrence rates of keloids and intractable hypertrophic scars in the anterior chest wall, as well as the scapular and suprapubic regions, were statistically higher than at other sites, while the recurrence rates in earlobes were lower. Thus, we customized doses for various sites. This report describes our trial of postoperative radiation therapy. METHODS: Between January 2002 and September 2004, 109 patients with 121 keloid and intractable hypertrophic scar sites were treated with surgical excision following the new protocol: electron-beam irradiation at total doses of 10, 15, or 20 Gy, depending on the site. The recurrence rates and toxicities were historically followed in 218 patients with 249 keloid and intractable hypertrophic scar sites treated with the old protocol of surgical removal followed by irradiation at 15 Gy (without variation by site). The minimal follow-up time was 18 months. Statistical analysis was performed using Fisher exact probability test. RESULTS: Total recurrence rates were 29.3% before 2002 and 14.0% after 2003. The recurrence rate in the anterior chest wall was statistically reduced. Outcomes of earlobe did not differ between irradiation with 15 Gy or 10 Gy. CONCLUSIONS: Keloids and intractable hypertrophic scars should be treated with dose protocols customized by site. Our results suggest that keloid and intractable hypertrophic scar sites with a high risk of recurrence should be treated with 20 Gy in 4 fractions over 4 days and that earlobe should be treated with 10 Gy in 2 fractions over 2 days.     

细胞信号传导在激素和干扰素诱导的增殖瘢痕成纤维细胞凋亡中的作用

目的 探讨对瘢痕疙瘩和增生性瘢痕成纤维细胞在激素和干扰素α-2b(IFNα-2b)作用后是否产生凋亡,以及相关细胞信号传导通路的激活或抑制是否一致.方法 对6例瘢痕疙瘩、增生性瘢痕及6例皮肤标本,采用细胞培养、免疫组织化学、凝胶电泳及FACE ELISA方法通过检测Bax和Bcl-2蛋白表达、特异性DNA梯状条带以及激活(磷酸化)的ERK1/2和JNK的吸光度A值,对不同成纤维细胞在地塞米松(0.1 mg/ml)和干扰素α-2b(1000U/ml)作用后的细胞凋亡及相关细胞信号传导通路进行了研究.结果 地塞米松可通过激活ERK1/2和JNK细胞传导通路诱导三类不同来源成纤维细胞发生细胞凋亡;干扰素α-2b不能诱导这三类不同来源成纤维细胞发生明显细胞凋亡,且IFN α-2b抑制增殖瘢痕的ERK1/2通路,而对JNK通路无影响,其不引起正常皮肤成纤维细胞ERK1/2和JNK通路的变化.结论 激素类药物和干扰素α-2b对瘢痕疙瘩、增生性瘢痕和正常皮肤成纤维细胞的作用机制不同.     

Treatment of hypertrophic scars and keloids: a review

Objective: The purpose of this study was to provide a review of the diagnosis and treatment of hypertrophic scars and keloids. Data Sources: A MEDLINE search was conducted for pertinent English-language articles published from 1966 to 1999. Study Selection: All studies concerning the pathophysiology and treatment of hypertrophic scars and keloids were reviewed. Data Extraction: Publications with clinically relevant data were selected for discussion in the article. Data Synthesis: Hypertrophic scars and keloids can pose a formidable therapeutic challenge. Numerous treatments are available. These include intralesional corticosteroids, topical applications, surgery, and, most recently, laser therapy. Silicone sheeting and cryotherapy are among the useful adjunctive agents for hypertrophic scar and keloid treatment. Vitamin E, onion extract derivative, and aloe vera have not proved to be effective. Surgery provides an invasive but sometimes necessary alternative in the treatment of scars. Radiation therapy may have a role in the treatment of recalcitrant lesions. Most recently, the pulsed-dye laser has been successfully used to treat keloids and hypertrophic scars. Conclusions: Currently, no definitive therapy exists for the treatment of keloids and hypertrophic scars. The advent of laser technology, particularly the pulsed-dye laser, appears to offer the best hope for successful treatment. Combination therapy seems to offer increased efficacy.