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Keloid scars tend to occur in high-tension sites due to mechanical stimuli that are involved in their development. To date, a detailed analysis of keloid distribution focused specifically on facial and neck areas has not been reported, and limited literature exists as to the related mechanical factors. To rectify this deficiency of knowledge, we first quantified the facial and neck keloid distribution observed clinically in 113 patients. Subsequently, we performed a rigorous investigation into the mechanical factors and their associated changes at these anatomic sites in healthy volunteers without a history of pathologic scarring. The association between keloid-predilection sites and sebaceous gland-dense and acne-prone sites was also examined. To assess skin stretch, thickness and stiffness, VECTRA, ultrasound and indentometer were utilised. Baseline skin stiffness and thickness were measured, as well as the magnitude of change in these values associated with facial expression and postural changes. Within the face and neck, keloids were most common near the mandibular angle (41.3%) and lateral submental (20.0%) regions. These areas of increased keloid incidence were not associated with areas more dense in sebaceous glands, nor linked consistently with acne-susceptible regions. Binomial logistic regression revealed that changes in skin stiffness and thickness related to postural changes significantly predicted keloid distribution. Skin stiffness and thickness changes related to prolonged mechanical forces (postural changes) are most pronounced at sites of high keloid predilection. This finding further elucidates the means by which skin stretch and tension are related to keloid development. As a more detailed analysis of mechanical forces on facial and neck skin, this study evaluates the nuances of multiple skin-mechanical properties, and their changes in a three-dimensional framework. Such factors may be critical to better understanding keloid progression and development in the face and neck., (© 2024 The Authors. Wound Repair and Regeneration published by Wiley Periodicals LLC on behalf of The Wound Healing Society.)

Background: The skin is a protective barrier of the body against external factors, and its damage leads to a loss of integrity. Normal wound healing results in a correct, flat, bright, and flexible scar. Initial skin damage and patient specific factors in wound healing contribute that many of these scars may progress into widespread or pathologic hypertrophic and keloid scars. The changes in cosmetic appearance, continuing pain, and loss of movement due to contracture or adhesion and persistent pruritis can significantly affect an individual's quality of life and psychological recovery post injury. Many different treatment methods can reduce the trauma and surgical scars. Manual scar treatment includes various techniques of therapy. The most effectiveness is a combined therapy, which has a multidirectional impact. Clinical observations show an effectiveness of manual scar therapy., Material and Methods: The aim of this work was to evaluate effectiveness of the scar manual therapy combined with complementary methods on the postoperative scars. Treatment protocol included two therapies during 30 min per week for 8 weeks. Therapy included manual scar manipulation, massage, cupping, dry needling, and taping., Results: Treatment had a significant positive effect to influence pain, pigmentation, pliability, pruritus, surface area, and scar stiffness. Improvement of skin parameters (scar elasticity, thickness, regularity, color) was also noticed., Conclusion: To investigate the most effective manual therapy strategy, further studies are needed, evaluating comparisons of different individual and combined scar therapy modalities., (© 2022 The Authors. Skin Research and Technology published by John Wiley & Sons Ltd.)

Long-term poor dietary habits can cause changes in the intestinal flora, resulting in the production of a large number of lipopolysaccharide, increase intestinal mucosal permeability, and activate the entrance of a large number of inflammatory factors into the portal vein. In addition, a high carbohydrate diet can increase liver metabolic burden, increase mitochondrial oxidative phosphorylation, leading to oxidative stress, generate new fat during adenosine triphosphate synthesis, and thus resulting in ectopic fat accumulation, which further activate nuclear factor-κB signaling pathway and release inflam- matory factors such as tumor necrosis factor-α, interleukin-1β (IL-1β), IL-6, and so on. This leads to obesity and insulin resis- tance, ultimately triggering systemic low-grade inflammation. This article reviews the mechanism of poor dietary habits leading to systemic low-grade inflammation, the clinical and experimental research progress of keloids and systemic low-grade inflammation, the association between dietary habits and keloid constitution, and puts forward the hypothesis that poor dietary habits may lead to the occurrence and development of keloids.

Pathogenic variation in the X-linked gene FLNA causes a wide range of human developmental phenotypes. Loss-of-function is usually male embryonic-lethal, and most commonly results in a neuronal migration disorder in affected females. Gain-of-function variants cause a spectrum of skeletal dysplasias that present with variable additional, often distinctive, soft-tissue anomalies in males and females. Here we present two, unrelated, male individuals with novel, intronic variants in FLNA that are predicted to be pathogenic. Their phenotypes are reminiscent of the gain-of-function spectrum without the skeletal manifestations. Most strikingly, they manifest urethral anomalies, cardiac malformations, and keloid scarring, all commonly encountered features of frontometaphyseal dysplasia. Both variants prevent inclusion of exon 40 into the FLNA transcript, predicting the in-frame deletion of 42 amino acids, however the abundance of FLNA protein was equivalent to that observed in healthy individuals. Loss of these 42 amino acids removes sites that mediate key FLNA functions, including binding of some ligands and phosphorylation. This phenotype further expands the spectrum of the FLNA filaminopathies., (© 2021 Wiley Periodicals LLC.)

The scratch assay is an in vitro technique used to analyze cell migration, proliferation, and cell-to-cell interaction. In the assay, cells are grown to confluence and then 'scratched' with a sterile instrument. For the cells in the leading edge, the resulting polarity induces migration and proliferation in attempt to 'heal' the modeled wound. Keloid scars are known to have an accelerated wound closure phenotype in the scratch assay, representing an overactivation of wound healing. We performed a qualitative review of the recent literature searching for inhibitors of scratch assay activity that were already available in topical formulations under the hypothesis that such compounds may offer therapeutic potential in keloid treatment. Although several shortcomings in the scratch assay literature were identified, caffeine and allicin successfully inhibited the scratch assay closure and inflammatory abnormalities in the commercially available keloid fibroblast cell line. Caffeine and allicin also impacted ATP production in keloid cells, most notably with inhibition of non-mitochondrial oxygen consumption. The traditional Chinese medicine, shikonin, was also successful in inhibiting scratch closure but displayed less dramatic impacts on metabolism. Together, our results partially summarize the strengths and limitations of current scratch assay literature and suggest clinical assessment of the therapeutic potential for these identified compounds against keloid scars may be warranted., Competing Interests: The authors have declared that no competing interests exist.

Background: Most of the widely used methods for the assessment of keloid treatment are subjective grading scales based on the opinion of an individual clinician or patient. There is a growing need for objective methods to evaluate keloid treatment., Objective: This study aimed to evaluate the value of laser speckle contrast imaging (LSCI) as an objective method for the assessment of dual-wavelength laser therapy for keloids., Methods: This prospective study included 21 patients with 54 keloids. All patients were treated with a combined 585-nm pulsed dye laser and 1,064 nm neodymium-doped yttrium aluminum garnet dual-wavelength laser at 4 weeks to 6 weeks intervals. Keloids were assessed using the Vancouver Scar Scale (VSS) and LSCI., Results: The total VSS score significantly decreased after 4 sessions of treatment (p < .05). Blood perfusion in keloids as measured by LSCI was significantly reduced after treatment (p < .05). The improvement of chest keloids in terms of the total VSS score and blood perfusion was significantly greater than that of scapular keloids (p < .05). There was a positive correlation between decreased perfusion and reduced total VSS score (R2 = 0.84)., Conclusion: Blood perfusion in keloids significantly decreased after dual-wavelength laser therapy. Laser speckle contrast imaging is a promising objective method for assessing the improvement of keloids treated with laser therapy., (Copyright © 2020 by the American Society for Dermatologic Surgery, Inc. Published by Wolters Kluwer Health, Inc. All rights reserved.)

Background: Keloid disease is hard to fully eradicate. Recurrence and other unsatisfactory results were found in many patients. No current therapeutic modality has been determined to be most effective for treating keloid scars. Intralesional corticosteroid injections is most commonly recommended for primary management of small and young keloids as well as hypertrophic scars. However, it's difficult for patients to adhere to long-term triamcinolone acetonide injection therapy because of the pain, inconvenience or complications including hormonal imbalance or irregular menstruation., Objective: We aimed to determine whether and how Strontium-90 brachytherapy as an adjuvant radiation could affect keloid recurrence after intralesional triamcinolone and 5-fluorouracil injections., Methods: We included keloid patients from March 2019 to September 2019 and randomly allocated them to two groups after 3 intralesional triamcinolone and 5-fluorouracil injections at 3 weeks interval. The experimental group received Strontium-90 brachytherapy at a total dose of 15-20Gy, while the control group didn't receive any adjuvant treatment. We performed both Vancouver Scar Scale scoring and Color Doppler ultrasound examination to monitor and evaluate lesions regularly. A one-year follow-up was completed for each patient., Results: 31 patients who had 42 keloids in total were recruited. We found intralesional triamcinolone and 5-fluorouracil injections could effectively reduce the thickness and modify the hardness of small and young keloids. Strontium-90 brachytherapy reduced the one-year recurrence rate from 85.7 percent to 44.4 percent after 3 intralesional triamcinolone and 5-fluorouracil injections. The lesions' thickness or elasticity was not affected by Strontium-90 brachytherapy., Conclusion: Strontium-90 brachytherapy as an adjuvant radiation could effectively reduce small sized keloids recurrence after intralesional triamcinolone and 5-fluorouracil injections. It worked by enhancing the lesions' stability post-injection., Trial Registration: The clinical trial registration number: ChiCTR2000030141. Name of trial registry: Chinese Clinical Trial Registry (http://www.chictr.org.cn/)., Competing Interests: The authors have declared that no competing interests exist.

Background: Recurrence rates of keloids have generally been reported at one time point. However, the longer the duration after treatment, the greater the likelihood that such lesions will recur. In this study, we analysed the time to recurrence during long-term follow-up., Material and Methods: We retrospectively reviewed recurrence-free interval in 52 patients with keloid (age 8-79 years) who had been treated between June 2006 and January 2011 using a standardised protocol developed by our group., Results: Mean duration of follow-up was 37.5 (range, 7-120) months in patients with keloid. Kaplan-Meier survival curves revealed a statistically significant difference in recurrence-free interval between ear keloids and keloids excluding ear keloids. Recurrence rate for keloids was high in the first 2 years after treatment., Conclusions: Kaplan-Meier analysis was useful for understanding the tendency of recurrence of keloids after treatment using a standardised protocol., (Copyright © 2020 Tissue Viability Society. Published by Elsevier Ltd. All rights reserved.)

Objectives: Collagen VI-related dystrophies (COL6-RDs) have a broad clinical spectrum and are caused by mutations in the COL6A1, COL6A2 and COL6A3 genes. Despite the clinical variability, two phenotypes are classically recognized: Bethlem myopathy (BM, milder form) and Ullrich congenital muscular dystrophy (UCMD, more severe form), with many patients presenting an intermediate phenotype. In this work, we present clinical and genetic data from 28 patients (27 families), aged 6-38 years (mean of 16.96 years), with COL6-RDs., Patients and Methods: Clinical, muscle histology and genetic data are presented. COL6A1, COL6A2 and COL6A3 genes were analyzed by next-generation sequencing (NGS)., Results: Homozygous or heterozygous variants were found in COL6A1 (12 families), COL6A2 (12 families) and COL6A3 (3 families). Patients with the severe UCMD phenotype (three cases) had a homogeneous clinical picture characterized by neonatal onset of manifestations, no gait acquisition and a stable course, but with severe respiratory involvement. Most of the patients with the mild UCMD phenotype had neonatal onset of manifestations (88.8 %), delayed motor development (66.6 %), slowly progressive course, pulmonary involvement (55.5 %) and loss of the walking capacity before the age of 10 (66.6 %). In the intermediate group (nine patients), some children had neonatal onset of manifestations (44.5 %) and delayed motor development (88.9 %); but all of them achieved the ability to walk and were still ambulatory. Some patients that had the BM phenotype presented neonatal manifestations (57.1 %); however, all of them had normal motor development and normal pulmonary function. Only one patient from the group of BM lost the walking capacity during the evolution of the disease. Other frequent findings observed in all groups were joint retractions, spinal deformities, distal hyperextensibility, congenital hip dislocation and keloid formation., Conclusion: COL6-RDs present variable clinical manifestations, but common findings are helpful for the clinical suspicion. NGS is a valuable approach for diagnosis, providing useful information for the genetic counseling of families., Competing Interests: Declaration of Competing Interest The authors declare that they have no conflict of interest., (Copyright © 2020 Elsevier B.V. All rights reserved.)

The purpose of this study was to investigate the performance of high-frequency ultrasound (HFUS) and shear wave elastography (SWE) in the quantitative evaluation of therapeutic responses of keloids. 43 patients with 76 keloids were recruited into this study. In keloids and symmetrical sites, the skin thickness was measured using HFUS and skin stiffness expressed as elastic moduli (Young's modulus and shear wave velocity) was measured using SWE. The coefficient of variation values were calculated by using difference values of skin elastic moduli and skin thickness. A significant increase of both skin stiffness and thickness appeared in pre-treated keloids compared with post-treated keloids (P < 0.001) and normal controls (P < 0.001), respectively. Stiffness in post-treated keloids and normal skins was significantly different (P < 0.001), while the difference in thickness measurements showed no significance (P = 0.56, >0.05). The coefficient of variation of Young's modulus was the highest when compared between (i) pre-treated keloids and theirs site-matched areas; (ii) pre-treated and post-treated keloids. SWE, which showed greater ability in determining the extent of keloids recovery, may provide an ideal tool to assess the stiffness of keloids and theirs therapeutic response.

Following injury, the skin undergoes a wound healing process culminating in the formation of a mature scar. Millions of patients worldwide are left with scars every year as a result of trauma or surgery. Scars can be painful, disfiguring and disabling, yet patients report that clinicians are often dismissive of their concerns, unable to identify pathological scars and unaware of treatment options. The normal wound healing process comprises three overlapping stages: inflammation, proliferation and remodelling. In some patients this process is deranged, resulting in the formation of hypertrophic or keloid scars. Clinicians can minimize the risk of these pathological scars developing with good surgical technique and wound aftercare. If pathological scars do form, they should be identified early and patients referred for treatment, most often topical or intralesional corticosteroids. In resistant cases, pathological scars may be treated with phototherapy, radiotherapy or surgical resection.

Background: Fibroproliferative disorders result in excessive scar formation, are associated with high morbidity, and cost billions of dollars every year. Of these, keloid disease presents a particularly challenging clinical problem because the cutaneous scars progress beyond the original site of injury. Altered mechanotransduction has been implicated in keloid development, but the mechanisms governing scar progression into the surrounding tissue remain unknown. The role of mechanotransduction in keloids is further complicated by the differential mechanical properties of keloids and the surrounding skin., Methods: The authors used human mechanical testing, finite element modeling, and immunohistologic analyses of human specimens to clarify the complex interplay of mechanical stress, strain, and stiffness in keloid scar progression., Results: Changes in human position (i.e., standing, sitting, and supine) are correlated to dynamic changes in local stress/strain distribution, particularly in regions with a predilection for keloids. Keloids are composed of stiff tissue, which displays a fibrotic phenotype with relatively low proliferation. In contrast, the soft skin surrounding keloids is exposed to high mechanical strain that correlates with increased expression of the caveolin-1/rho signaling via rho kinase mechanotransduction pathway and elevated inflammation and proliferation, which may lead to keloid progression., Conclusions: The authors conclude that changes in human position are strongly correlated with mechanical loading of the predilection sites, which leads to increased mechanical strain in the peripheral tissue surrounding keloids. Furthermore, increased mechanical strain in the peripheral tissue, which is the site of keloid progression, was correlated with aberrant expression of caveolin-1/ROCK signaling pathway. These findings suggest a novel mechanism for keloid progression.

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.)

Background: Hyperbaric oxygen therapy (HBOT) has been widely used in the clinical setting. In this study, HBOT therapy was evaluated for its ability to ameliorate the epithelial-to-mesenchymal transition (EMT) phenomenon in keloid tissue., Methods: Keloid patients were randomly divided into two groups: keloid patients (K group, 9 patients) and keloid patients receiving HBOT (O group, 9 patients). A third group with normal skin (S group, 9 patients) was established for control. Before HBOT and surgery, a laser Doppler flowmeter was used to measure the keloid blood supply of patients in the O group. Hematoxylin and eosin (H&E) staining was used to observe morphology. E-cadherin, ZO-1, vimentin, fibronectin, vascular endothelial growth factor (VEGF), and hypoxia inducible factor (HIF)-1α were measured by immunofluorescence staining and Western blot analysis. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to evaluate the mRNA expression level of these factors as well., Results: In the O group, keloid blood perfusion was significantly reduced after patients received HBOT. Compared with the K group, lower expression levels of vimentin, vibronectin, VEGF, and HIF-1α were observed in the O group, whereas the expression of E-cadherin and ZO-1 was significantly higher. The mRNA expression of E-cadherin and ZO-1 was also increased after HBOT., Conclusions: The expression levels of factors related to the EMT phenomenon were significantly reversed in keloid patients after they received HBOT, indicating that HBOT may be an effective therapy against the EMT phenomenon in keloid patients.

Background: Human adipose tissue-derived mesenchymal stem cells (ASCs) have potential utility as modulators of the regeneration of tissue that is inflamed or scarred secondary to injuries such as burns or trauma. However, the effect of ASCs on one particular type of scarring, keloidal disease, remains unknown. The absence of an optimal model for investigation has hindered the development of an effective therapy using ASCs for keloids., Objective: To investigate the influence of ASCs on angiogenesis, extracellular matrix deposition, and inflammatory cell influx in keloids., Methods: We analyzed the proliferation, migration, and apoptosis of human keloid-derived fibroblasts treated with a starvation-induced, conditioned medium from ASCs (ASCs-CM). This was achieved by Brdu proliferation assay, a validated co-culture migration assay, and flow cytometry, respectively. To assess the change in phenotype to a pro-fibrotic state, fibroblasts were analyzed by real-time PCR and contraction assay. A keloid implantation animal model was used to assess the paracrine effect of ASCs histochemically and immunohistochemically on scar morphology, collagen deposition, inflammatory cell composition, and blood vessel density. In tandem, an antibody-based array was used to identify protein concentration in the presence of ASCs-CM at time point 0, 24, and 48h., Results: ASCs-CM inhibited the proliferation and collagen synthesis of human keloid-derived fibroblasts. ASCs-CM was associated with reduced inflammation and fibrosis in the keloid implantation model. Thirty-four cytokines were differentially regulated by ASCs-CM at 24h. These included molecules associated with apoptosis, matrix metalloproteases, and their inhibitors. The same molecules were present at relatively higher concentrations at the 48h timepoint., Conclusion: These results suggest that ASCs are associated with the inhibition of fibrosis in keloids by a paracrine effect. This phenomenon may have utility as a therapeutic approach in the clinical environment., (Copyright © 2017 Elsevier Ltd and ISBI. All rights reserved.)

Treatments for keloid scarring are a major challenge to scientists and physicians for their unknown aetiology. Although several models, including monolayer cell culture to tissue-engineered models, were developed, further research on keloid has more or less been hindered by the lack of appropriate animal models. Because these aberrant scars are specific to humans, we obtained human normal and keloid skin tissues and isolated dermal fibroblasts from them. Cell morphology, growth and immunohistochemical staining of myofibroblastmarker α-SMA were examined, and the cell medium of 2-hour culture and 24-hour culture was implanted on the back of nude mice. The cell medium of 2-hour culture and 24-hour culture was also analysed by a protein array for the detection of distinction in inflammatory factors. We showed that keloid fibroblasts had similar morphology and growth compared to normal skin fibroblasts, but the α-SMA expression was obviously up-regulated. After 6 weeks, mice of the 2-hour keloid-derived culture medium group exhibited keloid-like hypertrophic nodules macroscopically, while mice of 24-hour keloid-derived culture medium group were similar to normal skin. Histological findings confirmed that the reconstituted skin tissues had the typical features of human keloids. The protein array data revealed that RANTES were involved in humanised fibrotic occurrence in mice, also suggesting they were important modulators of this inflammatory event. This novel model might help to understand the key events that result in the formation of these abnormal scars and provide new therapeutic options., (© 2017 Medicalhelplines.com Inc and John Wiley & Sons Ltd.)

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.

The molecular mechanism of the pathogenesis of keloids is still not known and the clinical management of keloids remains challenging. MiRNA (microRNA) is a novel class of small regulatory RNAs that has emerged as key post-transcriptional regulators of gene expression. MiRNAs participate in diverse biological processes of various skin diseases and function as key regulators in the occurrence and development of tumors. The purpose of this study was to investigate the involvement of miRNAs in keloid pathogenesis. We performed miRNA microarray analysis to compare miRNA expression between keloid and normal skin samples. We found that 46 miRNAs were upregulated and 28 miRNAs were downregulated in keloid compared with normal skin samples. We focused on miR-1224-5p, which has been reported to function in cancers, although the expression and mechanism of miR-1224-5p in keloids remain to be explored. Overexpression of miR-1224-5p led to inhibition of keloid fibroblast proliferation, promotion of apoptosis and decrease of migration and invasion. Our results suggest that downregulation of miR-1224-5p may be one of the mechanisms involved in the occurrence and development of keloids., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Epithelial-mesenchymal transition (EMT) plays a critical role in fibrotic keloid formation, which is characterized by excessive collagen and extracellular matrix synthesis and deposition. Growing evidence suggests that the serine/threonine kinase homeodomain-interacting protein kinase 2 (HIPK2) acts upstream of several major fibrosis signaling pathways; however, the role of HIPK2 in the keloid fibrogenesis remains unknown. In the current study, we investigated the roles of HIPK2 in the pathogenesis of keloids. Primary normal skin and keloid keratinocytes were cultured and pretreated with transforming growth factor (TGF)-β1. Next, keratinocytes were transfected with scrambled small interfering RNA (siRNA) and anti-HIPK2 siRNA. The TGF-β1-associated HIPK2 alterations were investigated by quantitative real-time polymerase chain reaction. Protein levels were analyzed by western blotting. The HIPK2 was markedly increased in the keloid-derived keratinocytes compared with normal skin keratinocytes. In addition, HIPK2 induced the expression of EMT markers in normal skin keratinocytes by TGF-β1-SMAD family member 3 (SMAD3). The effect of TGF-β1-related EMT markers and SMAD3 phosphorylation in response to added TGF-β1 was significantly abrogated when the cells were transfected with HIPK2 siRNA. We conclude that HIPK2 is a crucial factor in the pathogenesis of keloids, suggesting that HIPK2 might be a novel potential drug target for antikeloid therapy.

Keloid is a cutaneous fibroproliferative disorder. It results from impaired wound healing that generates persistent inflammation and extensive deposition of collagen fibers in the wound/scar. Keloids tend to be worse in hypertensive patients. The present prospective cross-sectional study assessed whether endothelial dysfunction, which occurs in hypertension, associates with keloid formation and progression. This study included randomly selected patients with keloids who were assessed for surgical keloid treatment in 2013-2014. A series of nonkeloid patients admitted to the hospital was also recruited during this period. To measure endothelial function, all patients underwent digital reactive hyperemia peripheral arterial tonometry. Test results were expressed as reactive hyperemia index (RHI) and augmentation index (AI). In total, 57 patients with keloids and 19 nonkeloid controls were recruited. Keloid patients did not differ from the controls in terms of demographic or clinical variables, but had significantly worse RHI and AI values. Moreover, poor RHI and AI values associated with keloid development on binomial logistic regression. The keloid patients were then divided into four groups depending on whether their keloids started at age 0-12, 13-18, 19-29, or ≥30 years. Patients whose keloids arose before and well after puberty tended to have lower RHI than the controls, but these differences did not achieve statistical significance. However, these two groups did have significantly poorer AI values than the controls. Thus, endothelial dysfunction could cause keloid formation and/or aggravation. This indicates that vascular endothelial cells are important for wound healing., (© 2017 by the Wound Healing Society.)

Keloids are fibroproliferative skin disorders characterised clinically by continuous horizontal progression and post-surgical recurrence and histologically by the accumulation of collagen and fibroblast ingredients. Till now, their aetiology remains clear, which may cover genetic, environmental and metabolic factors. Evidence in the involvement of local mechanics (e.g. predilection site and typical shape) and the progress in mechanobiology have incubated our stiffness gap hypotheses in illustrating the chronic but constant development in keloid. We put forward that the enlarged gap between extracellular matrix (ECM) stiffness and cellular stiffness potentiates keloid progression. Matrix stiffness itself provides organisational guidance cues to regulate the mechanosensitive resident cells (e.g. proliferation, migration and apoptosis). During this dynamic process, the ECM stiffness and cell stiffness are not well balanced, and the continuously enlarged stiffness gap between them potentiates keloid progression. The cushion factors, such as prestress for cell stiffness and topology for ECM stiffness, serve as compensations, the decompensation of which aggravates keloid development. It can well explain the typical shape of keloids, their progression in a horizontal but not vertical direction and the post-surgical recurrence, which were evidenced by our clinical cases. Such a stiffness gap hypothesis might be bridged to mechanotherapeutic approaches for keloid progression., (© 2016 Medicalhelplines.com Inc and John Wiley & Sons Ltd.)

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.

Scarring is the response elicited by the skin surface to injury and loss of tissue material. Wound healing takes place through a complex natural repair system consisting of vascular, inflammatory and proliferative phenomena, followed by a remodelling and cell apoptosis phase. This incredible repair system is inevitable, but sometimes unpredictable due to individual differences based on multiple factors. The scar is the objective criterion of a skin surgery, both for the patient and the dermsurgeon. It is therefore crucial to establish with the patient during the preoperative consultation, the size and positioning of the expected scar, taking into account the oncologic, anatomic and surgical constraints. Scars can ideally blend into normal skin, but may also give rise to various abnormalities. We can manage and prevent these abnormalities by mastering initial inflammation, that may induce hyperpigmentation and hypertrophy. Early massage using cortocosteroid topic or anti-inflammatory moisturizers may be effective. Random individual scarring may be minimized by a dynamic personalized accompanying scarring., (© 2016 Elsevier Masson SAS. Tous droits réservés.)

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.)

Background and Objectives: Keloids are fibroproliferative lesions of unknown origin that are characterized by increased collagen deposition. Vascularization may play a role in the pathogenesis of keloids, but existing reports are contradictory. Thus, we assessed perfusion within keloids and surrounding skin using laser speckle contrast imaging (LSCI)., Study Design/materials and Methods: Twenty-one patients with 61 untreated keloids were enrolled into this study. LSCI was used to evaluate blood flow in the keloids and surrounding skin. Three regions of interest were manually defined: keloids (K), skin adjacent to keloids (A), and nonadjacent skin separated by at least 0.3 cm from the edge of the keloids (N). Mean perfusion in each of these regions was determined and ratios (K/N, A/N) were calculated., Results: Significantly higher perfusion was noted in keloids and adjacent skin compared with nonadjacent skin (P < 0.05). The mean values (95% confidence intervals) of the ratios were: K/N = 2.41 (2.28-2.54) and A/N = 1.33 (1.28-1.37). A heterogeneous perfusion map was frequently observed. Mean perfusion in keloids and nonadjacent skin in the chest region was significantly higher than that on the back (P < 0.05). There was no statistical signficant difference in K/N at different locations (P > 0.05)., Conclusions: Perfusion values in keloids and adjacent skin were significantly higher than those in nonadjacent skin. LSCI may be a suitable and useful way of assessing perfusion in keloids., (© 2016 Wiley Periodicals, Inc.)

Recently, thymic stromal lymphopoietin (TSLP), which is well studied in allergic diseases, has been reported in fibrotic diseases, including idiopathic pulmonary fibrosis and atopic dermatitis fibrosis. However, the role of TSLP in keloid is obscure. In this study, we assessed the expression of TSLP in keloid tissue and investigated the possible role of TSLP in keloid pathogenesis. We observed that TSLP expression was increased in keloid tissue compared to normal tissue. Furthermore, TSLP treatment induced increased collagen I and collagen III expression in fibroblasts via transforming growth factor-?; however, there was higher expression in keloid fibroblasts compared to normal fibroblasts. Stromal cell-derived factor-1?, which was recently reported to enhance wound healing through recruiting bone marrow-derived mesenchymal stem cells to the wound area, increased after TSLP treatment in fibroblasts and was primarily expressed in ?-smooth muscle action-positive myofibroblasts in keloid tissue. Furthermore, fibrocytes expressing CXCR4, a stromal cell-derived factor-1? receptor, were significantly increased in keloid tissue compared to normal tissue. Finally, intradermal TSLP injection on BALB/c mice increased stromal cell-derived factor-1? expression and CXCR4(+) fibrocytes infiltration. Our data suggest that TSLP is a potent inducer of collagen and transforming growth factor-? production in keloid fibroblasts. In addition, it might activate the CXCR4/stromal cell-derived factor-1 axis to increase fibrocyte infiltration into the keloid tissue., (Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: The regulation of apoptosis, proliferation, and migration of fibroblasts is altered in keloids. The 90-kDa heat shock protein (heat shock protein 90) is known to play a key role in such regulation. Therefore, the authors investigated whether the inhibition of heat shock protein 90 in keloid fibroblasts could induce apoptosis and attenuate keloid fibroblast proliferation and migration., Methods: The authors evaluated heat shock protein 90 expression in keloid tissues with immunohistochemistry. The authors used cell viability [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assays and annexin V/propidium iodide staining for apoptosis, a wound healing model and cell tracking system to assess cell migration, and Akt Western blotting analysis in keloid fibroblasts after inhibition of heat shock protein 90 with 17-allylaminodemethoxygeldanamycin (17-AAG)., Results: The expression of heat shock protein 90 in keloid tissues was significantly increased compared with normal tissues. The 17-AAG-treated keloid fibroblasts showed significantly decreased proliferation, promotion of apoptosis, and decreased expression of Akt. Furthermore, a dose-dependent decrease in cell migration was noted after 17-AAG treatment of keloid fibroblasts. The 17-AAG-treated keloid fibroblasts had less directionality to the wound center and migrated a shorter distance., Conclusions: The authors confirmed that the inhibition of heat shock protein 90 in keloid fibroblasts could promote apoptosis and attenuate proliferation and migration of keloid fibroblasts. Therefore, the authors think that the inhibition of heat shock protein 90 is a key factor in the regulation of biological processes in keloids. With further preclinical study, the authors will be able to apply these results clinically for keloid treatment.

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 defined as overgrowths of scar tissue resulting from abnormal wound healing. They are characterized by excessive dermal deposition of thick, hyalinized collagen bundles resulting from an imbalance between the production and degradation of extracellular matrix (ECM) components. Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) are two important regulators of ECM degradation and remodeling. To evaluate the role played by knockdown of TIMPs in keloid formation, we transduced human keloid-derived fibroblasts (KFs) with small interfering RNAs targeting TIMP-1 or -2 (siTIMP-1 or siTIMP-2) using a lentiviral vector and assessed the biological effects. We found that MMP-1/TIMP-1 and MMP-1/TIMP-2 complexes were suppressed and that MMP-2 activity was upregulated in KFs expressing siTIMP-1 or siTIMP-2. In addition, increased degradation of collagen type I was observed in the supernatant of KFs expressing siTIMP-1, but not siTIMP-2, with the suppression of cell viability and induction of apoptosis. These results suggest that targeting TIMP-1 using small interfering RNA has significant therapeutic potential as an approach to treating keloids through degradation of their thick collagen bundles.

Keloid formation of the plantar region is rare and a unique challenge to surgeons. We used a conservative "wait and see" approach for recurrent keloid in the plantar region in two patients and recommended that the patients used custom-made shoes. Both patients were pleased with the result. The keloids regressed and flattened. During our minimum of five years follow-up the patients had no pain, tenderness, paraesthesiae, or problems with walking. We found no complications. Keloids should not be treated aggressively, and in plantar keloids the conservative "wait and see" approach may provide successful results without any complication.

Keloid is a disease that is difficult to cure because of its high recurrence rate after chemotherapy or radiotherapy, therefore it is considered as a benign skin tumor. Tumor stem cells are proposed as the source for tumor development and post-therapy recurrence. Interestingly, keloid stem cells have also been discovered, which share some characters with those of skin progenitor cells. Keloid patients possess specific diathesis including genetic predisposition and gene mutation, abnormal levels of hormones, growth factors and cytokines, and strong inflammatory response. This article reviews related literatures and hypothesizes that keloid stem cells might be transformed from normal dermal progenitor cells in the pathological niche of keloid tissues. These keloid stem cells are highly self-renewal and drug resistant, and can sustain themselves by asymmetric division, and continually generate new keloid cells to replenish the cells killed by drugs or radiation, thus leading to over growth of keloid and high post-therapy recurrence rate., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Keloids behave like benign tumors as they grow beyond the boundaries of the original wound margin, do not regress spontaneously, and recur despite treatments. Recently, accumulating evidences showed that survivin played an important role in cell growth, apoptotic resistance, and cell cycle control. More than that, survivin was confirmed to be associated with tumor angiogenesis and chemoresistance. Survivin blocker therapy has been proved to be a novel treatment in some kinds of tumors. Our preliminary work showed that survivin expression was significantly higher in keloids than in normal skin. The mRNA and protein levels of survivin were downregulated in keloid fibroblasts by survivin-siRNA. Therefore, we hypothesize that survivin has a profound effect on keloid formation and progression. Therefore, survivin may be a potential therapeutic target for keloids. Our hypothesis sheds light for the first time on the role of survivin involves in keloid pathophysiology and provides with novel therapeutic implications for keloids that are associated with apoptosis., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Keloids are common cutaneous pathological scars that are characterised by the histological accumulation of fibroblasts, collagen fibres, and clinically significant invasive growth. Although increasing lines of research on keloids have revealed genetic and environmental factors that contribute to their formation, the etiology of these scars remains unclear. Several studies have suggested the involvement of lipid metabolism, from a nutritional point of view. However, the role that lipid metabolism plays in the pathogenesis and progression of keloids has not previously been reviewed. The progress that has been made in understanding the roles of the pro- and anti-inflammatory lipid mediators in inflammation, and how they relate to the formation and progression of keloids, is also outlined. In particular, the possible relationships between mechanotransduction and lipid metabolites in keloids are explored. Mechanotransduction is the process by which physical forces are converted into biochemical signals that are then integrated into cellular responses. It is possible that lipid rafts and caveolae provide the location of lipid signaling and interactions between these signaling pathways and mechanotransduction. Moreover, interactions between lipid signaling pathway molecules and mechanotransduction molecules have been observed. A better understanding of the lipid profile changes and the functional roles lipid metabolism plays in keloids will help to identify target molecules for the development of novel interventions that can prevent, reduce, or even reverse pathological scar formation and/or progression.

A skin scar is the sign of tissue repair following damage to the skin. Once formed, it follows a process of maturation which, after several months, results in a mature scar. This can be pathological with functional and/or aesthetic consequences. It is important to assess the scar as it matures in order to adapt the treatment to its evolution.

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.)

Keloid disease (KD) is a fibroproliferative disorder of unknown etiopathogenesis with ill-defined treatment. There is increasing evidence to suggest that aberrant Notch signaling may contribute directly to skin pathogenesis and altered expression of Notch receptors identified in KD. Therefore, the aim of this study was to investigate the Notch signaling pathway in KD compared to normal skin (NS). In this study, we employed in vitro primary cell culture models to elucidate the role of Notch signaling in 44 tissue samples from patients with KD split into keloid and extralesional (EL) samples (internal control) from the same patients, and six NS tissue samples (external control). We show the presence of a significant (p < 0.05) up-regulation of Notch receptors and ligand Jagged-1 (JAG-1) in KD compared to EL and NS tissue samples. Cell spreading, attachment, and proliferation were significantly (p < 0.05) reduced in JAG-1 antisense-treated primary dermal fibroblasts isolated from KD and treated with γ-secretase inhibitor (blocks proteolytic cleavage and activation of Notch), evaluated by real-time cell analyzer (RTCA) on a microelectronic sensory array. In contrast, extralesional skin fibroblasts (ELF) treated with recombinant human JAG-1 (rh-JAG-1) peptide showed significant (p < 0.05) enhancement of cell spreading, attachment, and proliferation in RTCA. Activation/inhibition of JAG-1 and Notch signaling significantly (p < 0.05) altered the behavior of primary keloid fibroblasts and ELF, in cell migration (using a scratch wound assay), invasion (using a 3D invasion assay), and angiogenesis (in vitro coculture tube formation assay). In conclusion, this is the first study to demonstrate a potential role for the Notch signaling pathway in KD progression and that targeting this pathway may provide a novel strategy for treatment of KD., (© 2012 by the Wound Healing Society.)

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.

Keloids are a fibroproliferative disease due to abnormal wound healing process after skin injury. They are characterized by overproduction of extracellular matrix (ECM) such as collagens. MicroRNAs (miRNAs) are noncoding small RNAs and negatively regulate protein expression. Several miRNAs that have critical roles in tissue fibrosis and ECM metabolism have been reported. However, regulation and function of miRNAs in keloid remain to be explored. The purpose of this study was to identify miRNAs involved in keloid pathogenesis. We performed miRNA microarray analysis to compare miRNA expression profiles between keloid-derived fibroblasts (KFs) and normal fibroblasts (NFs). In all, 7 upregulated and 20 downregulated miRNAs were identified. Among these, we focused on miR-196a, which showed the highest fold change. Overexpression or knockdown of miR-196a led to a decreased or increased level of secreted type I/III collagens, respectively. Reporter analysis showed direct binding of miR-196a to the 3' untranslated region (UTR) of COL1A1 and COL3A1. In conclusion, we demonstrate for the first time that miRNA expression profile is altered in KFs compared with NFs. Downregulation of miR-196a may be one of the mechanisms by which collagens are highly deposited in keloid tissues. Our findings suggest that miR-196a could be a new therapeutic target for keloid lesions.

Aims and Objectives: To review the current mechanisms and biologic processes leading to the formation of pathologic scars., Materials and Methods: A computerised literature search was carried out using MEDLINE for all published articles on ''pathologic scarring''. The medical subject headings ''scarring'' were combined with ''mechanisms''. A review of selected relevant literature was then undertaken., Results: Scarless embryonal healing tends to be characterised by minimal inflammatory reaction mediated by reduced IL6,IL8 and hyaluronidase while there are elevated levels of hyaluronic acid MMP1to3, as well as IL10.The multifunctional cytokine TGF-B, its several isoforms as well as its postreceptor signalling mechanisms appears to play the key role in the scarring process . There is also evidence to show that PDGF, IGF and other cytokines regulate scarring . While conventional antiscarring agents target the fibroplasia phase, others such as tamoxifen ,calcium channel blockers, and imidazolaquinolines targets various phases of the scarring process ., Conclusion: It appears that multiple mechanisms are involved in the phenotypical appearance of abnormal scarring. A deeper understanding of these mechanisms is pivotal to the development of better antiscarring therapies in the very near future .

Keloids are benign tumours composed of fibrous tissue produced during excessive tissue repair triggered by minor injury, trauma or surgical incision. Although it is recognized that keloids have a propensity to form in the upper torso of the body, the predisposing factors responsible for this have not been investigated. It is crucial that the aetiopathoical factors implicated in keloid formation be established to provide guidelines for well-informed more successful treatment. We compared keloid-prone and keloid-protected skin, identified pertinent morphological differences and explored how inherent structural characteristics and intrinsic factors may promote keloid formation. It was determined that keloid prone areas were covered with high tension skin that had low stretch and a low elastic modulus when compared with skin in keloid protected areas where the skin was lax with a high elastic modulus and low pre-stress level. Factors contributing to elevated internal stress in keloid susceptible skin were the protrusion of hard connective tissue such as bony prominences or cartilage into the dermis of skin as well as inherent skin characteristics such as the bundled arrangement of collagen in the reticular dermis, the existent high tension, the low elastic modulus, low stretch ability, contractile forces exerted by wound healing fibroblastic cells and external forces. Stress promotes keloid formation by causing dermal distortion and compression which subsequently stimulate proliferation and enhanced protein synthesis in wound healing fibroblastic cells. The strain caused by stress also compresses and occludes microvessels causing ischaemic effects and reperfusion injury which stimulate growth when blood rich in growth factors returns to the tissue. The growth promoting effects of increased internal stress, primarily, and growth factors released by reperfusing blood, manifest in keloid formation. Other inherent skin characteristics promoting keloid growth during the late stages of wound healing in the upper torso are the thinner epidermis, the presence of vellus hairs, the absence of protective immunoglobulin A (IgA), and the thick fragile quality of upper torso skin. As it is not known why there is a predilection for keloids to form in the upper torso of the body, this hypothesis implicating and associating inherent morphological characteristics and elevated stress in the aetiopathogenesis of keloids is of potential value in terms of prevention, management and treatment of these enigmatic tumours., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Keloids tend to occur on highly mobile sites with high tension. This study was designed to determine whether body surface areas exposed to large strain during normal activities correlate with areas that show high rates of keloid generation after wounding. Eight adult Japanese volunteers were enrolled to study the skin stretching/contraction rates of nine different body sites. Skin stretching/contraction was measured by marking eight points on each region and measuring the change in location of the marked points after typical movements. The distribution of 1,500 keloids on 483 Japanese patients was mapped. The parietal region and anterior lower leg were associated with the least stretching/contraction, while the suprapubic region had the highest stretching/contraction rate. With regard to keloid distribution, there were 733 on the anterior chest region (48.9%) and 403 on the scapular regions (26.9%). No keloids were reported on the scalp or anterior lower leg. Because these sites are rarely subjected to skin stretching/contraction, it appears that mechanical force is an important trigger that drives keloid generation even in patients who are genetically predisposed to keloids. Thus, mechanotransduction studies are useful for developing clinical approaches that reduce the skin tension around wounds or scars for the prevention and treatment of not only keloids but also hypertrophic scars., (© 2012 by the Wound Healing Society.)

In this report we highlight the use of PET scan in plastic and reconstructive surgery. PET scanning is a very important tool in plastic surgery oncology (melanoma, soft-tissue sarcomas and bone sarcomas, head and neck cancer, peripheral nerve sheath tumors of the extremities and breast cancer after breast esthetic surgery), as diagnosis, staging, treatment planning and follow-up of cancer patients is based on imaging. PET scanning seems also to be useful as a flap monitoring system as well as an infection's imaging tool, for example in the management of diabetic foot ulcer. PET also contributes to the understanding of pathophysiology of keloids which remain a therapeutic challenge.