Keloid Research Articles

NEDD4L Inhibits the Proliferation and Migration of Keloid Fibroblasts by Regulating YY1 Ubiquitination-Mediated Glycolytic Metabolic Reprogramming.

Keloid scarring is a complex fibroproliferative disorder characterised by excessive fibroblast proliferation. Inhibition of cellular glycolysis effectively suppresses the proliferation of keloid fibroblasts (KFs). Neural precursor cell-expressed developmentally downregulated gene 4-like (NEDD4L), a ubiquitin ligase, regulates cell proliferation in different diseases. This study investigated the effects of NEDD4L on glucose metabolism, proliferation and migration in KFs. Primary KFs were isolated from keloid skin tissues obtained from patients with active-stage keloids. Cell transfection was used to upregulate or downregulate NEDD4L and Yin Yang 1 (YY1) in KFs. Protein expression was assessed by immunohistochemistry and western blotting. The viability, proliferative capacity and migration ability of KFs were evaluated using the MTT method and the EdU and wound healing assays, respectively. The regulatory effect of NEDD4L on YY1 ubiquitination was examined by coimmunoprecipitation. The interaction between YY1 and hexokinase 2 (HK2) was confirmed by a dual-luciferase reporter assay. NEDD4L was downregulated, whereas YY1 and HK2 were highly expressed in keloid tissues compared with normal skin. Overexpression of NEDD4L inhibited the proliferation and migration of KFs. NEDD4L promoted YY1 degradation in KFs by inducing its ubiquitination. Upregulation of YY1 induced glucose consumption and lactate production in KFs via the transcriptional regulation of HK2. Increased expression of YY1 reversed the reduced viability, proliferation, and migration of KFs overexpressing NEDD4L. YY1 also reversed the NEDD4L-induced inhibition of glucose consumption and lactate production in KFs. Additionally, an invivo study confirmed the inhibitory roles of NEDD4L overexpression and YY1 knockdown in keloid formation. NEDD4L suppressed the viability, proliferation and migration of KFs by regulating YY1 ubiquitination-mediated glycolysis through HK2. These findings suggest a novel regulatory axis, NEDD4L/YY1/HK2, that mediates glucose metabolism in keloid formation.

A Novel Splice Site Variant in COL6A1 Causes Ullrich Congenital Muscular Dystrophy in a Consanguineous Malian Family.

Congenital muscular dystrophies (CMDs) are diverse early-onset conditions affecting skeletal muscle and connective tissue. This group includes collagen VI-related dystrophies such as Ullrich congenital muscular dystrophy (UCMD) and Bethlem myopathy (BM), caused by mutations in the COL6A1, COL6A2 and COL6A3 genes. We report a consanguineous Malian family with three siblings affected by UCMD due to a novel homozygous splice site variant in the COL6A1 gene. After obtaining consent, three affected siblings and their relatives underwent physical examinations by specialists and laboratory tests where possible. DNA was extracted from peripheral blood for genetic testing, including Whole Exome Sequencing (WES). Putative variants were confirmed through Sanger Sequencing and assessed for pathogenicity using in silico tools. The three siblings and their healthy parents, from a consanguineous marriage, presented with early-onset progressive muscle weakness, walking difficulty, proximal motor deficits, severe muscle atrophy, hypotonia, skeletal deformities, joint hyperlaxity, ankyloses at the elbows and knees, keloid scars and dental crowding. No cardiac involvement was detected and creatine kinase (CK) levels were normal. All had low serum calcium levels, treated with oral supplements. Needle myography indicated myopathic patterns. WES identified a novel splice site variant in the first intron of COL6A1 (c.98-1G>C), which segregated with the disease within the family. This variant is predicted to cause exon 2 skipping in COL6A1, with a high CADD score of 33 and Splice AI predicting it as deleterious. We identified a novel COL6A1 variant in a consanguineous family, highlighting the need for further studies in larger African cohorts to enhance genetic epidemiology and prepare for future therapeutic research.

Systematic Review: Keloid and Hypertrophic Scar Management Updates

Keloids and hypertrophic scars pose significant challenges in clinical management due to their propensity for recurrence and their impact on patient’s quality of life. This systematic review evaluates the efficacy of various treatment modalities for these scars, with an emphasis on clinical outcomes, symptom alleviation, and recurrence rates. A comprehensive literature search identified studies published between 2014 and 2024, encompassing randomized controlled trials and observational studies. Results indicate that advanced therapies, such as botulinum toxin type A (BTX-A) and platelet-rich plasma (PRP), exhibit superior outcomes compared to traditional treatments, including triamcinolone acetonide (TAC), particularly concerning scar appearance and safety profiles. Furthermore, combination therapies, such as intralesional cryotherapy and CO2 fractional laser with intense pulsed light (IPL), demonstrated promising results in enhancing scar reduction and patient satisfaction. This review underscores the necessity of personalized treatment strategies tailored to individual patient requirements, taking into account factors such as scar characteristics and skin types. Future research should concentrate on optimizing treatment regimens to maximize efficacy while minimizing adverse effects, thereby ensuring long-term success in the management of keloids and hypertrophic scars.

The effect of BCG revaccination on the response to unrelated vaccines in urban Ugandan adolescents (POPVAC C): an open-label, randomised controlled trial

Immune responses induced by several important vaccines differ between populations, with reduced responses in low-income and rural settings compared with high-income and urban settings. BCG immunisation boosts immune responses to some unrelated vaccines in high-income populations. We aimed to test the hypothesis that BCG revaccination can enhance responses to unrelated vaccines in Ugandan schoolchildren. We conducted an open-label, randomised controlled trial to compare the effects of BCG revaccination versus no BCG revaccination on the immunogenicity of subsequent unrelated vaccines among adolescents aged 13-17 years who are participants in an urban Ugandan birth cohort study, in which BCG vaccination was documented at birth. Participants were excluded if they had received any of the trial vaccines or related agents when aged 5 years or older. Computer-generated 1:1 randomisation was implemented in REDCap. Participants were excluded if they were concurrently enrolled in other trials; had a clinically significant history of immunodeficiency, or serious psychiatric conditions or moderate to severe acute illnesses; were taking immunosuppressive medications; had allergies to vaccine components, a predisposition towards developing keloid scarring; positive HIV tests or pregnancy tests; were female participants who were lactating; or if they planned to use investigational drugs, vaccines, blood products, or any combination thereof. Trial participants assigned to the BCG revaccination group received the live parenteral BCG-Russia vaccine (Serum Institute of India, Pune, India; 0·1 mL intradermally, right upper arm) at week 0. All participants received yellow fever vaccine (YF-17D; Sanofi Pasteur, Lyon, France; 0·5 mL intramuscularly, left upper arm), live oral typhoid vaccine (Ty21a; PaxVax, London, UK; one capsule per day taken for three alternate days), and quadrivalent virus-like particle human papillomavirus (HPV) vaccine (Merck, Rahway, NJ, USA; 0·5 mL intramuscularly, left upper arm) at week 4; and toxoid vaccines (tetanus-diphtheria; Serum Institute of India; 0·5 mL intramuscularly, left upper arm) and an HPV booster at week 28. An additional HPV vaccination at week 8 was provided to female participants older than 14 years who had not previously been vaccinated. The primary outcomes were yellow fever neutralising antibody titres at 4 weeks post-YF-17D vaccination, Salmonella enterica serovar Typhi (henceforth S Typhi) O-lipopolysaccharide (O:LPS)-specific IgG concentration at 4 weeks post-Ty21a vaccination, and HPV-16 and HPV-18 L1 protein-specific IgG concentration at 4 weeks post-HPV vaccination. Primary outcome assays were conducted at week 8, and at week 52 for tetanus-diphtheria. We conducted an intention-to-treat analysis comparing log-transformed outcomes between trial groups, with results back-transformed to geometric mean ratios (GMRs). The safety population comprised all randomly allocated participants. The trial was registered at the ISRCTN Registry (ISRCTN10482904) and is complete. Between Aug 31 and Oct 12, 2020, we screened 376 potential participants for eligibility. We enrolled and randomly allocated 300 participants to the two groups (151 [50%] to the BCG group and 149 [50%] to the no BCG group). 178 (59%) of 300 participants were male and 122 (41%) were female. 142 (91%) of 151 participants in the BCG group and 139 (93%) of 149 in the no BCG group completed follow-up. There was no effect of BCG revaccination, compared with no BCG revaccination, on the response observed for any vaccine. Yellow fever plaque reduction neutralising reference tests (PRNT50) titres (the reciprocal of the last plasma dilution that reduced by 50%) had a GMR of 0·95 (95% CI 0·75-1·19; p=0·62) and PRNT90 (reciprocal of the last plasma dilution that reduced by 90%) had a GMR of 0·94 (0·74-1·19; p=0·60); IgG to S Typhi O:LPS was 0·99 (0·80-1·23; p=0·94); IgG to HPV-16 was 0·97 (0·69-1·35; p=0·85) and to HPV-18 was 1·03 (0·76-1·40; p=0·83); and toxoid-specific IgG for tetanus was 1·13 (0·87-1·47; p=0·36) and was 1·00 (0·87-1·16; p=0·97) for diphtheria. There were no serious adverse events in either group. We found no evidence that BCG revaccination is an effective strategy to improve immunogenicity of other vaccines in this low-income, urban setting. UK Medical Research Council. For the Luganda translation of the abstract see Supplementary Materials section.

СОВРЕМЕННОЕ ЛЕЧЕНИЕ РУБЦОВОЙ ДЕФОРМАЦИИ ТКАНЕЙ

The problem of scar treatment is one of the most widespread in modern medicine. Treatment of scar formations is one of the most difficult tasks, as there is no single standard that is favorable in terms of efficacy and safety despite the active development in this area of research. Currently, conservative methods of treatment of scar tissue deformities such as corticosteroid administration, botulinum therapy, cryotherapy, microneedling, as well as surgical excision in combination with therapeutic methods are widely used, due to which the most favorable result is achieved. This study is devoted to the study of various modern methods of correction of hypertrophic and keloid scars that are becoming widespread in medicine, their comparison and identification of important advantages and disadvantages in order to choose the most effective treatment technique. Currently used conservative methods of treatment allow to cope with the problem of scar formations, but due to the high incidence of side effects, there is a tendency to search for the combined use of each of them, including with surgical excision to prevent the development of recurrences and to achieve a pronounced cosmetic effect and satisfaction among patients. Thanks to the constant development of medicine and the improvement of various methods, each patient can receive a personalized treatment approach that is guaranteed to reduce aesthetic discomfort due to the existing pathology, which is the main and important aspect of scar correction.

A Rare Cutaneous Manifestation of Systemic Sclerosis.

Nodular scleroderma can be a diagnostic challenge due to its rarity and wide clinical presentation, which can mimic other medical conditions such as keloid or hypertrophic scar, storiform collagenoma, sclerotic dermatofibroma or sclerosing perineuroma.Clinicians should have a high degree of suspicion for nodular scleroderma when a patient presents with firm nodular or keloidal skin lesions, to diagnose and treat it appropriately.It is important to recognise nodular scleroderma early because timely and accurate diagnosis is crucial for appropriate management to prevent severe debilitation and scleroderma-related complications, and to improve patient outcomes.

An Update on Molecular Mechanisms of Scarring-A Narrative Review.

Fibroblasts, the principal cellular mediators of connective tissue remodeling, play a crucial role in the formation of physiological and pathological scars. Understanding the intricate interplay between fibroblasts and other cellular and molecular components is essential for elucidating the underlying mechanisms driving scar formation. Hypertrophic scars, keloids and atrophic scars arise from dysregulated wound healing processes characterized by persistent inflammation, aberrant collagen deposition, and impaired extracellular matrix remodeling. Fibroblasts play a central role in the pathogenesis of such pathological scars, driving aberrant extracellular matrix remodeling, subsequently contributing to the formation of raised or depressed fibrotic lesions. The investigation of complex interactions between fibroblasts and the microenvironment is crucial for developing targeted therapeutic interventions aimed at modulating fibroblast activity and improving clinical outcomes in patients with pathological scars. Further research into the molecular pathways governing fibroblast behavior and their heterogeneity holds promise for advancing scar management strategies. This narrative review was performed to shed light on the mechanisms behind scar formation, with a special focus on the role of fibroblasts in the formation of different types of scars, providing insights into the pathophysiology of these conditions. Through the analysis of current knowledge, this review seeks to identify the key cellular and molecular mechanisms involved in fibroblast activation, collagen synthesis, and extracellular matrix remodeling in hypertrophic scar, keloid, or atrophic scar formation.

Decoding skin mysteries: Unveiling the link between microbiota and keloid scars through a Mendelian randomization study.

The cause of keloids remains unclear, but studies suggest a link between skin microbiota and keloid formation. However, the causal relationship has not been confirmed. This study utilized Genome-Wide Association Studies (GWAS) data from 2 population-based German cohorts, comprising a total of 1656 skin samples. To bolster the reliability of our results, we incorporated GWAS data from 3 keloid cohorts, encompassing 2555 patients and 870,556 controls (GWAS ID: keloid1, ebi-a-GCST90018874; keloid2, bbj-a-131; keloid3, ebi-a-GCST90018654). Subsequently, we employed bidirectional 2-sample Mendelian randomization (MR) analysis to probe the causal relationship between the variables. The primary method employed was the inverse-variance weighted (IVW) method, supported by heterogeneity analysis, horizontal pleiotropy testing, outlier detection, and "leave-one-out" sensitivity analysis. By synthesizing the results from 3 groups of MR analyses, we discovered a negative causal association between a.ASV063 [Finegoldia (unc.)] located on the volar forearm and keloid disease (IVW (keloid1) odds ratio (OR): 0.939, 95% confidence interval (CI): 0.886-0.994, P = .032; IVW (keloid2) OR: 0.897, 95% CI: 0.813-0.990, P = .031; IVW (keloid3) OR: 0.900, 95% CI: 0.825-0.981, P = .017). Similarly, a negative causal relationship may also exist between the genus: Bacteroides from the antecubital fossa and keloid disease (IVW (keloid1) OR: 0.928, 95% CI: 0.884-0.973, P = .002; IVW (keloid2) OR: 0.891, 95% CI: 0.820-0.968, P = .007; IVW (keloid3) OR: 0.918, 95% CI: 0.849-0.992, P = .030). Additionally, no reverse causation was found, with all analyses showing no signs of horizontal pleiotropy or heterogeneity. This study offers new insights for the prevention and treatment of keloids.

Efficacy of Nd:YAG Laser and Intralesional Triamcinolone Injection Combination Therapy in the Postoperative Management of Keloids.

Keloids, characterized by protruding scars that extend beyond the original skin damage site, cause significant emotional stress and reduced quality of life. Their exact pathogenesis remains unclear, with various hypotheses including growth factor imbalances and extracellular matrix changes. No single treatment is universally accepted, but multiple modalities like triamcinolone acetonide injection (TAC), laser therapies, and surgery are commonly used. This retrospective study involved East Asian patients who underwent keloid scar excision between March 2019 and June 2022. Patients were divided into two groups: one receiving only TAC injections and the other a combination of TAC and Nd:YAG laser therapy. The efficacy of treatments was evaluated using the modified Vancouver Scar Scale (mVSS) and the Patient and Observer Scar Assessment Scale (POSAS), with follow-ups at six and twelve months after operation. The study involved 111 patients. Both treatment groups showed significant improvements in mVSS and POSAS scores, but the combination therapy group demonstrated a statistically significant improvement in POSAS scores and lower recurrence rates at 12months compared to the TAC-only group. However, there was no significant difference in patient satisfaction between the groups. Dual therapy involving TAC injection and Nd:YAG laser treatment was more effective than TAC injection alone for managing keloid scars after surgery. This combination therapy showed better outcomes in preventing keloid recurrence and improving scar status at 12months after operation, along with significant improvements in patient-reported outcomes. This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

Future Directions About Keloid Scars Based on Pathogenesis and Therapies.

Keloids are pathologic scars that pose a significant functional and cosmetic burden. While the literature on keloid management continues to expand, the absence of standardized guidelines or treatment protocols endorsed by academic governing bodies remains a significant challenge. The pathogenesis of keloid scars is not fully elucidated. This review delves into the intricate pathogenesis of keloids, exploring the molecular and cellular mechanisms underlying their formation. Conventional therapies are analyzed in-depth considering their efficacy and limitations, including surgical excision, pharmacotherapies, radiotherapy, cryotherapy, silicone-based product, pressure therapy, and light-based therapy. The emergence of novel therapeutic approaches is discussed, including pharmacotherapies, physical therapies, and biological therapies, shedding light on their potential in treating keloid scars. We also contemplate future directions in the field, encompassing the application of targeted therapies, gene-editing tools, tissue engineering, and regenerative medicine, together with psychosocial support and patient education. In synthesizing current knowledge, scrutinizing therapeutic modalities, and envisioning future avenues, this review aims to provide a comprehensive reference for clinicians, researchers, and stakeholders engaged in the intricate field of keloid management.

Investigating the impact of botulinum toxin type a on the migration of normal human dermal fibroblasts: An invitro wound healing assay.

Botulinum toxin A (BoNT-A) is widely utilized in the management of hypertrophic and keloid scars. One proposed mechanism for scar prevention involves the inhibition of fibroblast migration in scars by BoNT-A. However, the data regarding the effect of BoNT-A on the migration of normal human dermal fibroblasts (NHDF) is limited. The aim of this study was to investigate the inhibitory effect of different types and dilutions of BoNT-A on the migration of NHDF. In vitro scratch wound assay, NHDF cells were cultured, incubated, and subjected to scratching using a sterile tip. Subsequently, the scratched NHDF monolayer was treated with different types of BoNT-A, including onabotulinumtoxinA (ONA), incobotulinumtoxinA (INCO), prabotulinumtoxinA (PRABO), or letibotulinumtoxinA (LETI), at varying concentrations of 10, 20, 25, 40, 50, and 100 units/milliliter (U/mL). Additionally, abobotulinumtoxinA (ABO) was administered at concentrations of 33, 50, 66, 71, 100, 150, 300, and 500 U/mL. Normal saline solution (NSS) served as a negative control. The extent of NHDF migration was evaluated by comparing each dilution of BoNT-A with the controls using high-content imaging at the 48-h time point. Furthermore, the viability of the of NHDF was assessed. The concentrations of 25, 40, and 50 U/mL of ONA (p < 0.001) and 25 U/mL of LETI (p < 0.05) demonstrated significantly inhibited NHDF migration in comparison to the control group. Conversely, all dilutions of PRABO, INCO, and ABO exhibited comparable NHDF migration to that of the control group. Regarding NHDF viability, no significant decrease was observed across any of the BoNT-A types and dilutions. Different types and dilutions of BoNT-A demonstrated variable inhibitory effects on NHDF migration invitro. The selection of BoNT-A formulation may significantly impact the clinical outcome of scar prevention related to fibroblast migration.

The Potential of Chat-Based Artificial Intelligence Models in Differentiating Between Keloid and Hypertrophic Scars: A Pilot Study.

Lasting scars such as keloids and hypertrophic scars adversely affect a patient's quality of life. However, these scars are frequently underdiagnosed because of the complexity of the current diagnostic criteria and classification systems. This study aimed to explore the application of Large Language Models (LLMs) such as ChatGPT in diagnosing scar conditions and to propose a more accessible and straightforward diagnostic approach. In this study, five artificial intelligence (AI) chatbots, including ChatGPT-4 (GPT-4), Bing Chat (Precise, Balanced, and Creative modes), and Bard, were evaluated for their ability to interpret clinical scar images using a standardized set of prompts. Thirty mock images of various scar types were analyzed, and each chatbot was queried five times to assess the diagnostic accuracy. GPT-4 had a significantly higher accuracy rate in diagnosing scars than Bing Chat. The overall accuracy rates of GPT-4 and Bing Chat were 36.0% and 22.0%, respectively (P = 0.027), with GPT-4 showing better performance in terms of specificity for keloids (0.6 vs. 0.006) and hypertrophic scars (0.72 vs. 0.0) than Bing Chat. Although currently available LLMs show potential for use in scar diagnostics, the current technology is still under development and is not yet sufficient for clinical application standards, highlighting the need for further advancements in AI for more accurate medical diagnostics. This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online instructions to authors www.springer.com/00266 .

The Causal Role of Uterine Fibroid in Keloid and Hypertrophic Scar: A Bidirectional Mendelian Randomization Study on European Populations.

The relationship between uterine fibroids and keloid/hypertrophic scars has been contradictory. Our research employs a bidirectional Mendelian Randomization (MR) approach to establish a clearer understanding of this potential causal link. This study aimed to determine the effect of uterine fibroids on keloid/hypertrophic scars and the effect of keloid/hypertrophic scars on uterine fibroids. We aimed to demonstrate the relationship between uterine fibroids and keloid/ hypertrophic scars. Our bidirectional MR study utilized summarized data from genome-wide association studies (GWAS) focused on European populations. Our primary tool for establishing causality was the Inverse-Variance Weighted (IVW) method. To reinforce the IVW findings, we also applied four alternative MR methods: MR-Egger, Maximum Likelihood, Weighted Mode, and Weighted Median. The IVW method indicated a significant causal link, with uterine fibroids greatly raising the likelihood of developing keloids (Odds Ratio [OR] = 1.202, 95% Confidence Interval [CI]: 1.045-1.381; P=0.010) and hypertrophic scars (OR = 1.256, 95% CI: 1.039-1.519; P=0.018). Parallel results were observed with the MR-Egger, Maximum Likelihood, Weighted Mode, and Weighted Median methods. Sensitivity analyses indicated robustness in these findings, with no evidence of heterogeneity or horizontal pleiotropy. Conversely, the reverse MR analysis did not demonstrate an increased risk of uterine fibroids due to keloids or hypertrophic scars. This study elucidates a significant causal effect of uterine fibroids on the development of keloid and hypertrophic scars, offering valuable insights into their pathogenesis and potential therapeutic targets.

Heterogeneity in Keloid Scars: Influence of Mechanical Stretching on Keloids Arising from Different Anatomical Sites

Heterogeneity in Keloid Scars: Influence of Mechanical Stretching on Keloids Arising from Different Anatomical Sites

51250 Public and Private Insurance Coverage of Keloid Scar Treatments

51250 Public and Private Insurance Coverage of Keloid Scar Treatments

3144: "Unlocking the Potential of Radiotherapy in Keloid Scar Treatment: A Holistic Assessment"

3144: "Unlocking the Potential of Radiotherapy in Keloid Scar Treatment: A Holistic Assessment"

Experimental Study of Ultra-Pulsed CO 2 Fractional Laser Combined With Recombinant Human Epidermal Growth Factor Gel in the Treatment of Eyelid Keloid.

Keloid (KD) and hypertrophic scars are prevalent and result from excessive growth of dermal tissue after skin damage. This review focused on the clinical application of the ultra-pulsed CO 2 fractional laser combined with recombinant human epidermal growth factor (rHEGF) gel in patients with eyelid KD. Patients (N = 98) with KD who underwent surgery were randomly divided into a study group (ultra-pulsed CO 2 fractional laser combined with rHEGF gel therapy, N = 49) and a control group (ultra-pulsed CO 2 fractional laser therapy, N = 49). Besides, 5 cases dropped out of the study, including 2 cases in the study group and 3 cases in the control group. Finally, 47 cases of the study group and 46 cases of the study group were included in the analysis. The clinical baseline data such as sex, age, body mass index, scar area, etiology, Vancouver Scar Scale score, Patient and Observer Scar Assessment Scale score, four-item itch questionnaire score, serum interleukin-6 (IL-6), IL-10, and tumor necrosis factor-α level expression were recorded in the study group (N = 47) and the control group (N = 46). There was no significant difference in gender, age, body mass index, scar area, etiology, Vancouver Scar Scale score, Patient and Observer Scar Assessment Scale score, 4-item itch questionnaire score, IL-6, IL-10, and tumor necrosis factor-α levels between the patients treated with ultra-pulse CO 2 fractional laser + rHEGF gel and those only treated with ultra-pulse CO 2 fractional laser ( p > 0.05). Vancouver Scar Scale scores, Patient and Observer Scar Assessment Scale scores, and four-item itch questionnaire scores of patients with eyelid KD decreased to a greater extent than those treated with ultra-pulsed CO 2 fractional laser combined with rHEGF gel ( p <0.01). Compared with ultra-pulsed CO 2 fractional laser treatment, ultra-pulsed CO 2 fractional laser combined with rHEGF gel was more efficacious in treating patients with eyelid KD, with a lower incidence of adverse effects and a 1-year recurrence rate. Ultra-pulsed CO 2 fractional laser combined with rHEGF gel can significantly improve the scar status and scar itching in patients with eyelid KD, with an obvious therapeutic effect, a low incidence of adverse effects, a 1-year recurrence rate, and high safety, which is worthy of popularization and application.

Comprehensive Insights into Keloid Pathogenesis and Advanced Therapeutic Strategies.

Keloid scars, characterized by abnormal fibroproliferation and excessive extracellular matrix (ECM) production that extends beyond the original wound, often cause pruritus, pain, and hyperpigmentation, significantly impacting the quality of life. Keloid pathogenesis is multifactorial, involving genetic predisposition, immune response dysregulation, and aberrant wound-healing processes. Central molecular pathways such as TGF-β/Smad and JAK/STAT are important in keloid formation by sustaining fibroblast activation and ECM deposition. Conventional treatments, including surgical excision, radiation, laser therapies, and intralesional injections, yield variable success but are limited by high recurrence rates and potential adverse effects. Emerging therapies targeting specific immune pathways, small molecule inhibitors, RNA interference, and mesenchymal stem cells show promise in disrupting the underlying mechanisms of keloid pathogenesis, potentially offering more effective and lasting treatment outcomes. Despite advancements, further research is essential to fully elucidate the precise mechanisms of keloid formation and to develop targeted therapies. Ongoing clinical trials and research efforts are vital for translating these scientific insights into practical treatments that can markedly enhance the quality of life for individuals affected by keloid scars.

Development of huge keloid at donor site and recurrent keloid at graft site after excision of pubic keloid followed by split-thickness skin graft: A case report.

Keloids are the result of abnormal tissue scarring that occur after skin injuries leading to pain, psychological distress, and impaired quality of life. Despite the high recurrence rate after surgical treatment, excision is often inevitable for symptom control. A 32-year-old female presented with a huge keloid on the pubic area accompanied by severe pain, pruritus, and infectious discharge. She also had multiple keloids on her chest and shoulders, indicating a strong predisposition to keloid formation. While high potential for recurrence was anticipated, surgical excision was inevitable for symptom control. Complete keloid excision followed by split-thickness skin graft was performed. Pathological report revealed keloid accompanied by ruptured epidermal inclusion cyst. Although postoperative care was highly recommended for prevention of keloid recurrence, the patient refused any additional management due to her financial difficulties. At postoperative 8 months, mild degree of keloid or hypertrophic scar at marginal area of the graft was observed, suggesting the potential sign of keloid recurrence. The patient voluntarily discontinued the outpatient follow-up for 2 years, and then returned with huge keloid not only at the graft site but also at the donor site. Keloid with inflamed epidermal inclusion cyst can cause severe pain where surgical excision is unavoidable, regardless of the high potential for recurrence. Additional postoperative care is necessary to prevent recurrence. Furthermore, attempts to minimize new keloid formation at the donor site after split-thickness skin graft, such as thin skin harvest or selecting the scalp as the donor site, should be considered.

Central centrifugal cicatricial alopecia is associated with keloid scarring in Black women: A retrospective chart review

Central centrifugal cicatricial alopecia is associated with keloid scarring in Black women: A retrospective chart review