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A large-scale online survey was designed to both inform and direct the development of an online community healthcare hub for people living with scarring. Focussed areas of questioning were generated to gather information on psychological symptoms, scar support and knowledge of wounds and healing. Simple statistical data was produced on the severity, aetiology and location of scarring. A secondary data analysis of the survey responses was conducted on more focussed themes. This survey was completed by 1034 people living with scars, 119 of which had burn scarring. The results highlight that patients with burn scars have higher levels of pre-existing psychological difficulties, carry a greater number of scars and experience more symptoms. A lack of support is identified for patients with scars once they have been discharged by their healthcare provider. The most popular forms of support were chosen as face-to-face interaction or online support. Key areas of support were found to be psychology particularly for help with acceptance or coping methods, wound care advice and meeting with other patients with scars. For these patients, key themes in the psychological impact of scarring include appearance-related concerns, social anxiety, acceptance and coping, experience of symptoms, skin viability and survivorship., (Crown Copyright © 2018. Published by Elsevier Ltd. All rights reserved.)

General Purpose: To provide information about the clinical presentation of hypertrophic scars and keloids based on their varied structural components., Target Audience: This continuing education activity is intended for physicians, physician assistants, nurse practitioners, and nurses with an interest in skin and wound care., Learning Objectives/outcomes: After completing this continuing education activity, you should be able to: ABSTRACT: Hypertrophic scars and keloids are firm, raised, erythematous plaques or nodules that manifest when the cicatrix fails to properly heal. They result from pathologic wound healing and often cause pain and decreased quality of life. The appearance of such cosmetically unappealing scars affects the confidence and self-esteem of many patients. These scars can also cause dysfunction by interfering with flexion and extension across joints. Both possess some unique and distinct histochemical and physiologic characteristics that set them apart morphologically and at the molecular level. While these entities have been the focus of research for many years, differentiating between them remains challenging for clinicians.This article reviews the clinical presentation of aberrant scars and illustrates how they can be differentiated. It outlines their pathophysiology and emphasizes the unique molecular mechanisms underlying each disorder. It also examines how altered expression levels and the distribution of several factors may contribute to their unique clinical characteristics and presentation. Further research is needed to elucidate optimal treatments and preventive measures for these types of aberrant scarring.

Background: Keloid and hypertrophic scars represent an aberrant response to the wound healing process. These scars are characterized by dysregulated growth with excessive collagen formation, and can be cosmetically and functionally disruptive to patients., Objective: Objectives are to describe the pathophysiology of keloid and hypertrophic scar, and to compare differences with the normal wound healing process. The classification of keloids and hypertrophic scars are then discussed. Finally, various treatment options including prevention, conventional therapies, surgical therapies, and adjuvant therapies are described in detail., Materials and Methods: Literature review was performed identifying relevant publications pertaining to the pathophysiology, classification, and treatment of keloid and hypertrophic scars., Results: Though the pathophysiology of keloid and hypertrophic scars is not completely known, various cytokines have been implicated, including interleukin (IL)-6, IL-8, and IL-10, as well as various growth factors including transforming growth factor-beta and platelet-derived growth factor. Numerous treatments have been studied for keloid and hypertrophic scars,which include conventional therapies such as occlusive dressings, compression therapy, and steroids; surgical therapies such as excision and cryosurgery; and adjuvant and emerging therapies including radiation therapy, interferon, 5-fluorouracil, imiquimod, tacrolimus, sirolimus, bleomycin, doxorubicin, transforming growth factor-beta, epidermal growth factor, verapamil, retinoic acid, tamoxifen, botulinum toxin A, onion extract, silicone-based camouflage, hydrogel scaffold, and skin tension offloading device., Conclusion: Keloid and hypertrophic scars remain a challenging condition, with potential cosmetic and functional consequences to patients. Several therapies exist which function through different mechanisms. Better understanding into the pathogenesis will allow for development of newer and more targeted therapies in the future.

Animal models are crucial for the study of fibrosis. Keloids represent a unique type of fibrotic scarring that occurs only in humans, thus presenting a challenge for those studying the pathogenesis of this disease and its therapeutic options. Here, several animal models of fibrosis currently in use are described, emphasizing recent progress and highlighting encouraging challenges., (Copyright © 2016 International Society of Matrix Biology. Published by Elsevier B.V. All rights reserved.)

We have yet to create a human scar model that demonstrates the complex nature of hypertrophic scar and keloid formation as well as ways to prevent them despite emerging advances in our understanding of the immune system, the inflammatory response, and proteomic and genomic changes after injury. Despite more complex in vitro models, we fail to explain the fundamental principles to scar formation, and the timeline of their development. The solution to developing the ideal in vitro scar model is one that mimics the heterogeneous cellular and molecular interactions, as well as the evolving structure and function of human skin., (© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Most cutaneous wounds heal with scar formation. Ideally, an inconspicuous normotrophic scar is formed, but an abnormal scar (hypertrophic scar or keloid) can also develop. A major challenge to scientists and physicians is to prevent adverse scar formation after severe trauma (e.g. burn injury) and understand why some individuals will form adverse scars even after relatively minor injury. Currently, many different models exist to study scar formation, ranging from simple monolayer cell culture to 3D tissue-engineered models even to humanized mouse models. Currently, these high-/medium-throughput test models avoid the main questions referring to why an adverse scar forms instead of a normotrophic scar and what causes a hypertrophic scar to form rather than a keloid scar and also, how is the genetic predisposition of the individual and the immune system involved. This information is essential if we are to identify new drug targets and develop optimal strategies in the future to prevent adverse scar formation. This viewpoint review summarizes the progress on in vitro and animal scar models, stresses the limitations in the current models and identifies the future challenges if scar-free healing is to be achieved in the future., (© 2014 The Authors. Experimental Dermatology. Published by John Wiley & Sons Ltd.)

Keloids are benign, fibroproliferative growths that occur as a result of dermal injury in ~15% of the population. They are characterized by their extension beyond the confines of the original injury and often present with pain and pruritus. Additionally, these growths may result in cosmetic deformities and contribute to significant emotional distress. It is thought that keloids form as a result of aberrancies in the normal wound-healing process, which is complex and involves an elegant interplay between multiple cell types, cytokines, and proteins. The exact etiology is unknown, but significant research efforts have been made. These efforts have revealed that various cell types in keloids are either hyperresponsive and/or overproductive of various growth factors. Additionally, keloid cell types respond differently to mechanical strain than skin cells in patients who do not form keloids. This lack of understanding of keloid pathophysiology has left the care provider with a lack of a single definitive treatment strategy. Instead, a multitude of therapies exist ranging from surgery to injectables to lasers and any combination thereof. This purpose of this article is to highlight our current knowledge and emerging scientific understanding of keloid pathology and the current management strategies., (Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.)

Minimizing scar size, width, and contour of elevation is a common goal for the facial plastic surgeon. Various standard techniques are employed to reduce tension and enhance the rapid and uneventful healing of incisions. In some cases, these routine measures are not judged to be adequate, and additional intraoperative and postsurgical measures are employed to control the body's innate healing processes. Mitomycin C and self-drying silicone gel have been particularity useful in our practice., (Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.)

Over the past two decades the treatment of hypertrophic scars and keloids has seen substantial changes due to the evolution of current and establishment of new conservative and surgical methods. This review gives an overview of the current research with respect to the multifactorial etiology and pathophysiology of keloids and hypertrophic scars, discusses conservative surgical treatment options and provides an outlook on novel treatment strategies.

Tissue regeneration repairs the fabric of the skin to maintain homeostasis after injury. The expression and proliferation of extracellular matrix (ECM) molecules in the dermis, mediated by a range of growth factors and cytokines, is a fundamental element of wound repair. Previous work focused on how these complex molecular mechanisms relate to the formation of raised dermal scars, including keloid and hypertrophic scars, characterized by excessive deposition of ECM molecules. However, the mechanisms in the wound repair pathway which lead to the differential expression and organization of ECM molecules observed in different types of scar tissue are not fully understood. To summarize what is known about the expression and composition of ECM molecules in abnormal scarring, an extensive search of the literature was conducted, focusing on keywords connected to skin scarring, hypertrophic scars and keloid disease. The transcription and translation of collagen I and III, fibronectin, laminin, periostin and tenascin are all increased in raised dermal scar tissue. However, hyaluronic acid, dermatopontin and decorin are decreased, and the expression and localisation of fibrillin and elastin fibres in the dermis are altered compared with normal skin and scars. Recent whole genome profiling and proteomic studies have led to the identification of regulatory elements with different expression profiles in hypertrophic and keloid tissue. If the mechanisms of raised dermal scar formation are to be elucidated and effective therapeutic treatments developed, an integrated approach to research is required, focussing on the interactions between ECM molecules, regulatory elements and pathways., (© 2011 The Authors. Journal of the European Academy of Dermatology and Venereology © 2011 European Academy of Dermatology and Venereology.)

The authors have developed a technique of disconnection of soft tissues using an ultrasound dissector for ablation of the changed by scar skin covering. The ultrasound dissector splits the subcutaneous adipose tissue and loose connective tissue without injuring the vascular-nervous bundles. This method substantially reduces the intraoperative blood loss. The complex treatment combining the little traumatic ultrasound dissector with conservative and physiotherapeutic methods of treatment and prophylactics allows considerable reduction of probability of recurrent pathological scars.

We use evidence-based algorithms to treat abnormal scarring, including keloids and hypertrophic scars (HSs). This involves a multimodal approach that employs traditional methods such as surgical removal, postoperative radiotherapy, corticosteroid injection, laser, and silicone gel sheets. As a result, the rate of abnormal scarring recurrence has decreased dramatically over the past 10 years. However, several problems remain to be solved. First, despite the optimization of a radiotherapy protocol, over 10% of cases who are treated with surgery and postoperative radiotherapy still recur in our facility. Second, the treatment options for cases with huge keloids are very limited. To address these problems, we performed basic research on the mechanisms that drive the formation of keloids and HSs. Extrapolation of these research observations to the clinic has led to the development of two treatment strategies that have reduced the rate of abnormal scar recurrence further and provided a means to remove large scars. Our finite element analysis of the mechanical force distribution around keloids revealed high skin tension at the keloid edges and lower tension in the keloid center. Moreover, when a sophisticated servo-controlled device was used to stretch wounded murine dorsal skin, it was observed that the stretched samples exhibited upregulated epidermal proliferation and angiogenesis, which are also observed in keloids and HSs. Real-time RT-PCR also revealed that growth factors and neuropeptides are more strongly expressed in cyclically stretched skin than in statically stretched skin. These findings support the well-established notion that mechanical forces on the skin strongly influence the cellular behavior that leads to scarring. These observations led us to focus on the importance of reducing skin tension when keloids/HSs are surgically removed to prevent their recurrence. Clinical trials revealed that subcutaneous/fascial tensile reduction sutures, which apply minimal tension on the dermis, are more effective in reducing recurrence than the three-layered sutures used by plastic surgeons. Moreover, we have found that by using skin flaps (e.g., perforator flaps and propeller flaps), which release tension on the wound, in combination with postoperative radiotherapy, huge keloids can be successfully treated.

Background: The physiopathogenesis of proliferative scarring in human skin is not well understood. Furthermore, knowledge of the precise mechanisms of action for physical treatment modalities is limited. Compression garments, occlusive/adhesive skin taping, and silicone gel sheets are applied to form an occlusion on the scar surface, reduce tension, and/or increase pressure on the scar itself. The mechanisms by which the external or superficial actions of these treatments cause remission of a protruding scar may be related to mechanoreceptor (nociceptor and cellular mechanoreceptor) responses., Methods: Basic research studies about mechanoreceptor-related (nociceptors and cellular mechanoreceptors, separately) events are reviewed and discussed based on proliferative scarring background. Scar management-related studies were corrected from the standpoint of mechanotransduction mechanisms. The methodologic quality of the clinical trials and basic studies was evaluated and reviewed., Results: It was suggested that many of the physical scar management methods, including compression therapy, silicone therapy, adhesive tape, and occlusive dressing therapy, are related to mechanotransduction mechanisms., Conclusions: A unifying perspective of basic research findings and clinical observations may be obtained by considering the mechanoreceptor-related events in scar management. Moreover, a precise understanding of the roles that cellular mechanoreceptors and mechanosensitive nociceptors play in proliferative scarring may lead to the development of innovative treatment strategies and new pharmacologic therapies targeting cellular mechanoreceptors and mechanosensitive nociceptors in fibroproliferative diseases.

Background: Hypertrophic scars and keloids result from an abnormal fibrous wound healing process in which tissue repair and regeneration-regulating mechanism control is lost. These abnormal fibrous growths present a major therapeutic dilemma and challenge to the plastic surgeon because they are disfiguring and frequently recur., Objective: To provide updated clinical and experimental information on hypertrophic scars and keloids so that physicians can better understand and properly treat such lesions., Methods: A Medline literature search was performed for relevant publications and for diverse strategies for management of hypertrophic scars and keloids., Conclusion: The growing understanding of the molecular processes of normal and abnormal wound healing is promising for discovery of novel approaches for the management of hypertrophic scars and keloids. Although optimal treatment of these lesions remains undefined, successful healing can be achieved only with combined multidisciplinary therapeutic regimens.

Keloids and hypertrophic scars are different forms of excessive dermal fibrosis thought to be caused by regulation of cellularity increase and decrease during the wound-healing process in predisposed individuals. Differences between keloids and hypertrophic scars include distinct clinical features, histologic evidence, and cellular function in response to molecular events. Keloids and hypertrophic scars are the results of increased fibroblast density and extracellular matrix substances. Interactions between epidermal keratinocytes and dermal fibroblasts play an important role in regulating tissue homeostasis and processing scar formation. Keloids and hypertrophic scars are the two different stages of the same process that is based on separate clinical and histochemical entities. The aim of this review is to provide updated information regarding similarities and differences between keloids and hypertrophic scars as two different sides of the same coin. This article will also enable the dermatologist to better understand fundamental biology of the scarring.

The mechanisms of fibroproliferation disease (FPD) of the skin, such as keloids and hypertrophic scars, are still unknown. Since mechanical stress appears to be an important factor for FPD generation, we have studied the intervening factors that connect mechanical stress with keloid and scar formation. Hence, we introduce our "neurogenic inflammation hypothesis" in this paper. Our hypothesis is as follows. Mechanical stress, including skin stretching, stimulates mechanosensitive nociceptors on sensory fibers in the skin. Stimulated fibers release neuropeptides, including SP and CGRP, and these peptides bind to the receptors SP-NK1R and CGRP-CGRP1R on various cells in the skin. Moreover, histamine release is upregulated by mast cells. Consequently, activated endothelial cells and vascular smooth muscle cells induce vasodilation and permeabilization of vessels. Cytokine production, including TGFbeta and NGF, is also stimulated by various cells. The neurogenic inflammation and upregulation of TGFbeta would activate fibroblasts through various signals. Interestingly, overexpressed NGF may induce the hyper-release of neuropeptides from sensory fibers, resulting in the accumulation of neuropeptides even in the absence of mechanical stress, once the malignant cycle has started. Moreover, individual differences in FPD generation may be based on differences in reactivity towards neuropeptides, NGF, and other neurotrophins. Hence, neuropeptide antagonists may be effective against FPD. While further experimental studies and clinical confirmation are needed, our hypothesis may provide new insights into the etiology and pathology of FPD of the skin, such as keloids and hypertrophic scars.

Aim: The treatment of keloid and hypertrophic scars remains a challenging clinical problem despite numerous proposed therapies reported in the literature. This is due to the fact that the mechanisms that bring about keloid/hypertrophic scars are not completely understood. This article reviews the pertinent literature regarding the pathophysiology and management of keloid and hypertrophic scars., Material and Methods: A computerized literature search using MEDLINE was conducted for published articles on keloid and hypertrophic scars. The medical subject headings "keloid" or "hypertrophic scar" were combined with "treatment" or "management" or "mechanisms" or "pathophysiology" using the Boolean operator "AND" to narrow the searches. A review of selected relevant literature was undertaken., Results: Numerous advances have been made in understanding the process of formation of wound healing and scar formation. This increased knowledge has led to the introduction of new treatments as well as to a better understanding of how older treatments work. These include surgical excision, intralesional steroid injection, cryotherapy, laser therapy, irradiation, mechanical compression dressing, silicone sheet applications, intralesional interferon injection, or combination of techniques. Many of the treatment modalities have a defined biologic basis while others are based on anecdotal reports., Conclusions: Presently there is still no single, reliable and effective treatment protocol for keloid and hypertrophic scars. However, surgical excision followed by postoperative intralesional steroid injection seems to provide a reasonable treatment outcome with low recurrence rate.

Scars are a natural part of dermal healing processes and consist of networks of fibrous collagen tissue, laid down in response to injury to the dermis. In some genetically susceptible individuals, the process of scar tissue formation is excessive, and there is an over-secretion of collagen. This causes the formation of benign tumours (raised) scars known as keloid and hypertrophic scars. Scars can have many significant functional, cosmetic and psychological sequelae. Steroids are used therapeutically in the management of abnormal scars; however, this is associated with a variety of adverse effects. Their intralesional administration is the most widely used and most effective treatment modality for raised skin scars today. Despite this, our understanding of the way in which they work is poor and literature on the topic is, to date, lacking. Further work is needed to clarify the exact mechanisms that bring about abnormal scarring, to aid our understanding of the disease and facilitate the development of more evidence-based treatment strategies.

Background: Expression of connexins and other constituent proteins of gap junctions along with gap junctional intercellular communication are involved in cellular development and differentiation processes. In addition, an increasing number of hereditary skin disorders appear to be linked to connexins. Therefore, in this report, the authors studied in vitro gap junctional intercellular communication function and connexin expression in fibroblasts derived from keloid and hypertrophic scar patients., Methods: Fibroblasts harvested from each of six keloid and hypertrophic scar patients were used for this study. Gap junctional intercellular communication function was investigated using the gap fluorescence recovery after photobleaching method, and expression of connexin proteins was studied using quantitative confocal microscopic analyses., Results: Compared with normal skin, a decreased level of gap junctional intercellular communication was seen in fibroblasts derived from hypertrophic scar tissue, whereas an extremely low gap junctional intercellular communication level was detected in fibroblasts derived from keloid tissue. We also detected little connexin 43 (Cx43) protein localized in fibroblasts derived from keloids. Moreover, Cx43 protein levels were much lower in fibroblasts derived from hypertrophic scars than in those derived from normal skin., Conclusions: The authors' data suggest that the loss of gap junctional intercellular communication and connexin expression may affect intercellular recognition and thus break the proliferation and apoptosis balance in fibroblasts derived from keloid and hypertrophic scar tissue.

Background: Lasers have been used in the treatment of hypertrophic scars and keloids for more than 20 years. Different laser systems have been examined; among them pulsed dye lasers are currently considered the laser of choice in these settings., Objectives: The purpose of this study is to review the pertinent literature and provide updated information on different laser therapies available for treatment of keloids and hypertrophic scars., Methods: A Medline literature search was performed for relevant publications., Results: In this review the results of published studies in the treatment and prevention of hypertrophic scars and keloids are presented. Suggested mechanisms of action are reviewed. A review of the optimal laser parameters to modulate treatment outcome will be discussed. Different lasers are effective in not only the treatment but also the prevention of hypertrophic scars and keloids, among them PDL is more promising. Most of the suggested theories are based on the selective photothermolysis in which the light energy emitted from a vascular laser is absorbed by hemoglobin, generating heat and leading to coagulation necrosis, neocollagenesis, collagen fiber heating with dissociation of disulfide bonds and subsequent collagen fiber realignment., Conclusion: The optimal laser is currently 585 nm PDL, although the recent results of Q-switched 532 nm frequency-doubled Nd:YAG are promising. Early use of lasers are beneficial, especially in those who are prone to develop these lesions.

Purpose of Review: The precise mechanisms of normal and abnormal scar formation have long remained a mystery despite the extensive literature regarding wound healing. Only recently have researchers begun to delineate the complex biochemical signaling pathways that regulate these processes. This article reviews basic wound healing, while focusing on medicine's latest understanding of the development and treatment of keloids and hypertrophic scars., Recent Findings: The importance of the transforming growth factor-beta signaling pathways and the related downstream effector molecules has proven to offer a new detailed view of scar biology. Regulation of scar metabolism with regards to collagen and wound matrix degradation is likewise showing promise in generating alternate therapies to treat abnormal scars., Summary: Understanding the exact process of normal and abnormal scar formation will help define better ways to successfully manage and potentially prevent abnormal healing like hypertrophic scars and keloids.

Background: Many studies have shown that up-regulation of angiotensin-converting enzyme (ACE) participates in adverse fibrous remodeling. Although this has become an accepted fact in the cardiovascular field, the relationship between ACE and cutaneous fibrous remodeling, such as keloid or hypertrophic scars, remains unknown., Objective: We sought to investigate ACE in normal skin, wounded skin, and pathologic scars., Methods: Ten samples undergoing a normal wound-healing process, 14 samples of pathologic scar tissue, and 15 samples of normal skin were used in this study. Cutaneous tissue ACE activities were measured with high-pressure liquid chromatography. Localization of ACE was assessed by immunohistochemistry., Results: The ACE activity in pathologic scar tissue was significantly higher than in normal and wounded skin. Immunohistochemical studies demonstrated that myofibroblasts were stained with anti-ACE antibody., Limitations: The study is small., Conclusions: These results suggest that up-regulated ACE may participate in cutaneous pathologic scar formation the same as the cardiovascular system.

Keloid and hypertrophic scars are the result of abnormal processes in scar formation. This paper reviews the literature and the many debates concerning the processes that cause abnormal scarring.

Objective: To disclose whether there is difference in nerve regeneration between human hypertrophic scars and keloids after deep burns so as to provide a basis for new clinical treatment., Methods: Fifty-seven samples that were clinically and pathologically diagnosed as hypertrophic scars or keloids after deep burns were examined by use of two-label immunohistochemistry to define the nerves in scars. Then, the Mean Integrated Optical Density (MIOD) of S-100 and the MIOD of neurofilament (NF) proteins were measured and analyzed., Results: In hypertrophic scars or keloids, the nerve regeneration was growing gradually. The speed was high 3-5 months after burn and it slowed down 18 months after burn. The expression of S-100 and NF varied with different period of time (P<0.05). The expression of S-100 and NF in hypertrophic scars was higher than that in keloids. There was no difference 3-5 months after burn, but there was difference 6 months after burn., Conclusion: S-100 and NF are good markers to define the nerve regeneration in scars. The nerve regeneration in hypertrophic scars or keloids changes with the times. The nerve regeneration is more conspicuous in hypertrophic scars than in keloids.

Keloid and hypertrophic scars are 2 types of excessive scarring observed clinically that require different therapeutic approaches. The clinical course and physical appearance define keloids and hypertrophic scars as separate entities; however, they are often confused because of an apparent lack of morphologic differences. Nevertheless, clinical differences between hypertrophic scars and keloids have long been recognized by plastic surgeons and dermatologists. Yet, translating these differences into morphologic or biochemical distinctions has prompted much conflict in the literature. The present report is an attempt to clarify the longstanding controversy regarding these 2 similar yet separate and nonidentical entities by highlighting the reported points of differentiation as well as the similarities.

This article examines the formation of abnormal scars and describes how the different types can be treated. Psychological issues may result from scarring. The authors discuss how nurses can help patients to come to terms with altered body image.

Background: Keloids and hypertrophic scars result from aberrant wound healing and remain a potential complication of any surgical procedure or trauma. Investigation of aberrant wound healing has been limited to the study of growth factors, collagen precursors, and DNA synthesis in simple in vitro systems, which necessitate removal or destruction of cells or factors in the growth environment of cell cultures. Multiphoton microscopy (MPM) can use endogenous chromophores such as collagen and nicotinamide adenine dinucleotide hydrogenase to produce thin optical sections of thick living tissues without the use of dyes or stains. Endogenous second-harmonic-generation (SHG) signals in collagen can be collected to form an MPM image., Objective: To present a novel wound-healing model used to investigate keloid-derived fibroblast activity and collagen production in the same intact tissue-engineered construct over time., Methods: Artificial tissue constructs called RAFTs (produced by suspension of keloid or normal dermal fibroblasts in type I collagen gel with an overlying keratinocyte layer) were cultured at air-fluid interface. Multiphoton microscopy SHG images of collagen in the intact tissue constructs consisting of normal or keloid-derived fibroblasts were obtained. The constructs were then incised with a scalpel. Serial MPM and phase-contrast microscopy images were obtained to monitor changes in the extracellular matrix in response to wounding of the artificial skin construct over 8 days., Results: The tissue-engineered constructs formed a bilayer resembling the dermis and epidermis of human skin. Phase-contrast microscopy revealed migration of keratinocytes into the defect created by scalpel wounding. The constructs were found to contract with time after wounding. The MPM SHG images showed collagen deposition in the tissue constructs after wounding. Tissue constructs with keloid-derived fibroblasts were found to deposit collagen at a higher rate than those with normal fibroblasts., Conclusions: The MPM model described herein permits serial observation of the same intact specimens without the need for fixation or cytotoxic stains. Furthermore, it demonstrates the biologic activity of RAFT artificial tissue constructs.

Today, wound management to avoid excessive scar formation is increasingly important, especially in populations with Fitzpatrick 3 or higher skin pigmentation. Medical science and industrial development are devoting more effort toward understanding and offering better therapy to control scars. However, advances in scar management have been hampered by the confusing or ambiguous terminology. There is no consensus on what amount of post-traumatic skin scar formation is "normal" and what should be considered "hypertrophic". In the World Health Organization's ICD-9, there is no diagnostic code for hypertrophic scar--only keloid is listed. Yet, the medical and scientific literature distinguishes them as different conditions. Our experience suggests that the diagnosis of keloid disease is greatly over-rendered. For black patients, an elevated scar seems, by default, diagnosed as keloid by most. This confusion results in inappropriate management of scar formation, and occasionally contributes to decision making related to elective or cosmetic surgery. Given that patients are expecting better outcomes from wound care today than in the past, this review article attempts to capture the essential biological factors related to wound scar production and discusses treatment options and indications used by the authors.

Both transepidermal water loss (TEWL) and skin surface high-frequency conductance are functions of the skin barrier. Systemic sclerosis (SSc) and hypertrophic scar (HS)/keloid are characterized by abnormal fibrotic changes in the dermis. Since the close interrelationship between the epidermis and the dermis has been well established, we analyzed the stratum corneum functions of forearm skin in 39 SSc patients after assessing the degree of the skin thickening and compared those functions with 10 age-matched normal controls. We also analyzed the stratum corneum functions of HS or keloid lesions in seven patients using the same methods, and compared those functions to adjacent or contralateral normal skin in identical patients. Neither the TEWL, nor high-frequency conductance of forearm skin in SSc patients were significantly different from those in normal controls. There was no correlation between the levels of TEWL or high-frequency conductance and the degree of skin thickening in SSc. In HS or keloid conditions, high-frequency conductance was significantly elevated (42.5+/-8.9 vs. 26.4+/-5.7, P<0.001). Although TEWL was elevated, there was no statistical significance (48.6+/-39.7 vs. 25.1+/-10.1). Our results revealed that stratum corneum functions are distinct between SSc and HS or keloid. This may reflect the various natures of dermal changes, which in turn differentiate the functions of the stratum corneum in the diseases.

Recent studies have suggested that the regulation of apoptosis during wound healing is important in scar establishment and the development of pathological scarring. In this study, we demonstrate that keloid fibroblasts can be identified as apoptotic cells because of their highly condensed chromatin and discrete nuclear fragments. To further reveal the phenomenon of apoptosis, we quantified the number of terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells in surgically resected tissues of keloids (N = 10), hypertrophic scars (N = 10), normal healed flat scars (N = 10), and dermatofibroma (N = 10). The number of TUNEL-positive cells was relatively low, but was significantly higher for the keloid group compared with the normally healed flat scar group (p = 0.004), suggesting reduced cell survival and increased apoptotic cell death in a subpopulation of keloid fibroblasts. Furthermore, the number of TUNEL-positive cells was significantly higher for the keloid group compared with the dermatofibroma group (p = 0.044), suggesting that a subpopulation of keloid fibroblasts may suppress tumorgenicity at a greater rate than dermatofibroma by undergoing cell death. Hypertrophic scars had significantly higher levels of apoptosis than normally healed flat scars (p = 0.033). Therefore, these results suggest that selected fibroblasts in keloids and hypertrophic scars undergo apoptosis, which may play a role in the process of pathological scarring.

Keloid and hypertrophic scars are a type of scarring pathology which is characterised by excess collagen deposition produced during the wound healing process. The mechanism by which this occurs is not understood and although hypertrophic scars can regress spontaneously, keloids do not, and currently no effective treatment exists. In this paper we hypothesise that nitric oxide, a free radical molecule synthesised by numerous mammalian cells, is involved in the formation of these scars. We suggest that the excess collagen production in keloid lesions can be attributed to higher than normal levels of nitric oxide, as the free radical is a known stimulus for fibroblast collagen synthesis. Furthermore, we propose that the basal epidermis is a source of this additional nitric oxide and we discuss this in relation to known histological characteristics of keloid and hypertrophic lesions., (Copyright 2001 Harcourt Publishers Ltd.)

Sucrose has been used to treat wounds with excellent results and with minimal abnormal scarring. In this study the effects of sucrose on collagen metabolism in fibroblast culture was evaluated. Sucrose (5.5, 15, or 25 mM) was added to granulation tissue, hypertrophic scar, and keloid fibroblast cultures, mRNA levels and procollagen aminopropeptides for type I and III collagens in cell culture medium were studied. Sucrose decreased mRNA levels for pro alpha 1(I) and pro alpha 1(III) collagens in fibroblast cultures derived from hypertrophic scar and keloid. In normal granulation tissue fibroblast cultures, 5.5 mM sucrose increased mRNA levels for pro alpha 1(I) and pro alpha 1(III) collagen, and higher concentrations decreased them. The synthesis of type I collagen decreased dose-dependently in all cell strains, whereas the synthesis of type III collagen decreased only in granulation tissue fibroblasts. To conclude, in vitro high concentrations of sucrose down-regulate both collagen gene expression and synthesis in normal granulation tissue fibroblasts, whereas in fibroblasts derived from abnormal scar sucrose down-regulates only type I collagen gene expression and synthesis, changing the pattern of collagen metabolism toward normal.

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.

Hypertrophic scars and keloids are a hyperproliferative response of connective tissue to trauma. Histologically the difference between the two is that keloids invade normal tissue whereas hypertrophic scars remain confined within the original wound. A variety of treatments have been proposed, which we will review according to their efficiency. Prevention of pathological scarring will also be discussed, and we will present our current attitude to treat these scars. As a surgical treatment for keloids, we have been using the intralesional technique which we think gives better results.

Keloids and hypertrophic scars represent exuberant forms of scar formation that frequently are pruritic, painful, and occasionally form strictures. As well, they may result in significant cosmetic disfigurement. Recent years have seen an increased understanding in the molecular and biological mechanisms of keloidal scar formation, allowing for the development of more specific therapeutic options for these lesions. Despite these developments, keloids and hypertrophic scars remain difficult to manage. Clinical, histopathological, and biochemical features of keloids and hypertrophic scars, as well as treatment guidelines, are discussed.

Silicone gel and silicone occlusive sheeting are widely used at present for the treatment of hypertrophic and keloid scars, without any scientific explanation as to their mode of action. In a recent paper the possibility was raised that static electricity generated by friction-activated silicone sheeting could be the reason for this effect, and that it can, with time, cause involution of hypertrophic and keloid scars. The objective of this study was to test this hypothesis and to observe whether a continuous and also an increased negatively charged static-electric field will shorten the treatment period. A device to implement these requirements gradually evolved over a 5-year period. A number of prototypes were tested until the final product was attained. Some of the patients in this study were treated initially with a silicone sponge inserted in the cushion. Later this version was changed to the final design described herein. A silicone cushion was developed with the purpose of increasing a negative static-electric charge to accelerate the regression process. The cushion is custom-made using a silicone occlusive sheeting envelope of 0.75-mm thickness, which does not deteriorate with use, and is partially filled with high viscosity silicone oil. Its edges are sealed, and its size is designed to extend a little beyond the scarred area. Static electricity readings, generated by activating the cushion by pumping action with the fingers, stretching or deforming the cushion, are invariably much higher when compared with those obtained with silicone occlusive sheeting and silicone gel sheeting. The interaction between the negatively charged ions of the cushion and the ionic charges of the tissue fluids may be the critical factor in achieving hypertrophic and keloid scars involution. Of the 30 patients enrolled in the study, 3 patients dropped out. Treatment with the silicone cushions yielded 63.3 percent cessation of itching and burning followed by pallor and flattening of the scar, some markedly so, over a few weeks to 6-month period. An additional 26.6 percent had their scars resolved in up to 12 months of treatment. Good contact of the cushion over the scar has been shown to be important in this clinical trial, and much creativity is needed for making elastic strap bindings that ensure this contact. The clinical trials extended over a 12-month period. Ten patients (33.3 percent) who had recalcitrant scars with little response to the use of the silicone cushion were given intralesional corticosteroid injections, in addition to the continued use of the cushion, resulting in a fairly rapid resolution of these scars over a period of months to a year.

Background: Many aspects related to the biology and the effective therapy of proliferative scars have remained undefined, in part due to a lack of an accurate and reproducible animal model with which to systematically study them. This report describes a new model for investigating the pathophysiology and manipulation of human proliferative scars., Materials and Methods: Human proliferative scars (n = 86) were explanted into flaps based on isolated vascular pedicles in congenitally athymic rats. Serial analysis of the structural and functional integrity of the explanted scars was performed by microscopy and by measurement of human procollagen type III peptide (PIIIP) production, human factor VIII immunostaining, and in vitro cellular proliferation., Results: By these methods, both fibroblastic and epithelial components of explanted scar specimens retained the histologic characteristics of original human scar specimens, for up to 12 months. Over the same duration, scar explants continued to have high levels of human PIIIP, comparable to those found in original surgical specimens. The microvasculature of scar explants demonstrated a double basement membrane, with no staining of human factor VIII in the inner capillary endothelial layer, suggesting that host vessels were growing into ghost vessels of the human donor scar. Human factor VIII staining decreased over time. Fibroblasts cultured from explanted scar demonstrated less aggressive growth characteristics than those from original surgical specimens., Conclusions: This new model is the first to allow such long-term maintenance and serial evaluation of human proliferative scar on an accessible, isolated vasculature. It may prove useful in further defining the biology and therapy of this widespread pathologic process.

Excess scar formation secondary to traumatic or surgical injuries can have devastating consequences, ranging from body disfigurement to organ dysfunction. Hypertrophic scars and keloids are skin fibrotic conditions that can be caused by minor insults to skin, such as acne or ear piercing, or by severe injuries such as burns. Differences between keloids, hypertrophic scars and normal scars include distinct scar appearance, histologic morphology and cellular function in response to growth factors. Recent advances in our understanding of the wound healing process reveal possible causes for hypertrophic scars and keloids. This information might assist in the development of efficacious treatment for hypertrophic scar and keloid formation.

Objective: To characterize the functional properties of the stratum corneum (SC) of various scars., Design: A prospective cohort study., Setting: University hospital medical center., Patients: Thirty-two consecutive patients surgically treated for various skin diseases and 26 consecutive patients with hypertrophic scars or keloids., Main Outcome Measures: Noninvasive bioengineering measurements of functional properties of the SC, such as transepidermal water loss (TEWL), high-frequency conductance, and SC turnover time., Results: The SC barrier function assessed by TEWL was found to be a better parameter for the functional evaluation of scars than the hydration state of the skin surface measured by high-frequency conductometry. In general, the SC on the scars of deeper wounds in the dermis took longer to normalize functionally than the SC on the scars of superficial wounds, especially on the high compared with the abdomen. Thus, elevated levels of TEWL observed on scars at the donor sites of split-thickness grafts normalized between 200 and 400 days in contrast to fewer than 50 days for those of subepidermal erosions. Both TEWL and high-frequency conductance remained high in hypertrophic scars and keloids, and the SC involved showed a faster turnover time than that of adjacent normal skin., Conclusions: Scars, a proliferative change of the dermis, can be objectively evaluated according to functional abnormalities of the SC, because the dermis has a close relationship with the epidermis and with the SC. The functional characteristics of the SC of fresh scars and those of hypertrophic scars and keloids resemble those of retinoid-treated skin, rather than those found in epidermal hyperproliferative conditions such as psoriasis and dermatitis.

Aberrant fibrous tissue formation after surgery or trauma still presents a challenge to surgeons. Current research hopes to identify the characteristics of the population of fibroblasts that lead to hypertrophic or keloid scar formation. Surgical procedures and laser therapy followed by intralesional steroid treatments still are the foundation of treatment; but new modalities are being applied. The pathogenesis and management of hypertrophic scars, keloids, and scar contractures are discussed in this article.

Despite the disfigurement and symptoms from these abnormal wound responses, the literature offers little consensus about appropriate therapy. Few prospective blinded studies have been performed to compare therapeutic options. Multiple therapies have been reported. Most physicians agree with Kelly's emphasis on the importance of prevention. All effort should be directed to avoid or to minimize any stimuli that could promote an abnormal wound response in predisposed individuals. Treatment must be carefully selected for appropriate lesions. Hypertrophic scars may be surgically corrected, but other measures such as intralesional corticosteroid injection, pressure therapy, cryotherapy, and other topical treatments may be useful. These scars have a different clinical course than do keloids. Published recurrence rates for keloid treatment are lowest for the combination of surgery and radiation. Although some keloids may respond to intralesional steroid injection, keloid tissue must be removed and the resulting wound must be treated to minimize the risk of recurrence.