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Keloids constitute an abnormal fibroproliferative wound healing response in which raised scar tissue grows excessively and invasively beyond the original wound borders. This review provides a comprehensive overview of several important themes in keloid research: namely keloid histopathology, heterogeneity, pathogenesis, and model systems. Although keloidal collagen versus nodules and α-SMA-immunoreactivity have been considered pathognomonic for keloids versus hypertrophic scars, conflicting results have been reported which will be discussed together with other histopathological keloid characteristics. Importantly, histopathological keloid abnormalities are also present in the keloid epidermis. Heterogeneity between and within keloids exists which is often not considered when interpreting results and may explain discrepancies between studies. At least two distinct keloid phenotypes exist, the superficial-spreading/flat keloids and the bulging/raised keloids. Within keloids, the periphery is often seen as the actively growing margin compared to the more quiescent center, although the opposite has also been reported. Interestingly, the normal skin directly surrounding keloids also shows partial keloid characteristics. Keloids are most likely to occur after an inciting stimulus such as (minor and disproportionate) dermal injury or an inflammatory process (environmental factors) at a keloid-prone anatomical site (topological factors) in a genetically predisposed individual (patient-related factors). The specific cellular abnormalities these various patient, topological and environmental factors generate to ultimately result in keloid scar formation are discussed. Existing keloid models can largely be divided into and systems including a number of subdivisions: human/animal, explant/culture, homotypic/heterotypic culture, direct/indirect co-culture, and 3D/monolayer culture. As skin physiology, immunology and wound healing is markedly different in animals and since keloids are exclusive to humans, there is a need for relevant human models. Of these, the direct co-culture systems that generate full thickness keloid equivalents appear the most promising and will be key to further advance keloid research on its pathogenesis and thereby ultimately advance keloid treatment. Finally, the recent change in keloid nomenclature will be discussed, which has moved away from identifying keloids solely as abnormal scars with a purely cosmetic association toward understanding keloids for the fibroproliferative disorder that they are.

There are many methods to treat keloid, including various excision operations, laser, injection and radiotherapy. However, few studies have explored the effectiveness of single-hole punch excision in keloid treatment. This study aimed to investigate the efficacy and safety of lateral punch excision combined with intralesional steroid injection for keloid treatment through self-control trial. In this self-controlled trial, 50 patients meet the diagnosis of nodular keloid, and try to choose left–right symmetrical control, one skin lesion in the control group (50 skin lesionsin total) and the other in the observation group (50 skin lesions in total).The keloids in the treatment group were initially treated with punch excision combined with intralesional steroid injection, followed by injection treatment alone. Keloids in the control group received intralesional steroid injection alone. The Vancouver Scar Scale (VSS) of the keloid before and after the punch excision was evaluated; the keloid scores at different time points and the number of injection treatments required in both groups were compared, and adverse reactions were observed. The effective rate of the observation group was 86.0%, which was significantly higher than that of the control group (66.0%), and the recurrence rate of 22% was lower than that of the control group (χ 2  = 4.141,63417), all of which were statistically significant (all P  < 0.05). At the end of treatment, the VSS and total injection times in the observation group were significantly lower than those in the control group (t = 5.900,3.361), with statistical significance ( P  < 0.01). The combination of single-hole punch excision and intralesional steroid injection is an effective method to treat multiple nodular keloids, shortening the treatment course of tralesional steroid injection without obvious adverse reactions.

Background Hypertrophic scars and keloids are human cutaneous fibroproliferative conditions that develop after burns, trauma, surgery, and inflammation. Vitamin D inhibits keloid fibroblast proliferation by reducing TGF‐β‐induced extracellular matrix formation, boosting matrix metalloproteinase activity, and reducing inflammation. Aim To study the effect of intralesional and systemic Vitamin D3 injection on hypertrophic scars and keloids and whether vitamin D3 deficiency increases scarring. Patients and Methods This study included 30 hypertrophic scars and keloid patients divided into groups depending on serum vitamin D levels. Every patient was tested for vitamin D using ELISA. Group I: patients with vitamin D deficiency or insufficiency received a systemic injection of vitamin D (cholecalciferol 200 000 I.U.) once monthly for 3 months with a calcium oral supplement and intralesional vitamin D injections on hypertrophic scars and keloids. Group II: patients with sufficient vitamin D received only intralesional vitamin D injections. Results Vitamin D deficiency did not affect scar formation or severity (total Vancouver scar scale before assessment) with a p value > 0.05. All instances showed a substantial drop in vascularity, pliability, and total Vancouver scale score (p value < 0.05) following intervention, but no change in scar pigmentation or height. Scar assessment following intervention did not significantly differ between research groups (p > 0.05). Conclusion Injection of vitamin on hypertrophic scars and keloids enhances vascularity and pliability in patients with sufficient serum vitamin D levels and those with deficient or insufficient serum vitamin D levels after improving them by systemic injection of vitamin D without any effect on height and pigmentation of scars. Trial Registration NCT06301178

Treatment of keloids (K) and hypertrophic scars (HTS) is challenging. A few case reports reported good results in HTS treated by fractional CO 2 laser. The aim of the present study was the assessment of the clinical response as well as histological changes in K and HTS treated by fractional CO 2 laser and the role of matrix metalloproteinase 9 (MMP9) in the response. A randomized half of the scar was treated by fractional CO 2 laser in 30 patients (18 K, 12 HTS) for a total of four sessions 6 weeks apart. Vancouver scar score (VSS) was done before and 1, 3, and 6 months after the last laser session by a blinded observer. Biopsies taken from normal skin, untreated scar, and treated scar tissue 1 and 3 months after the laser sessions were stained by HX & E for histological changes and Masson trichrome for collagen fiber arrangement. Immunohistochemical staining for MMP9 was done in before and 1 month after samples. Quantitative morphometric analysis was done for collagen and MMP9 by image analyzer. Nineteen patients completed the 6-month follow-up period (12 K, 7 HTS). VSS score was significantly lower in the treated compared to untreated areas after 3 and 6 months in both K and HTS but was mainly due to improved pliability of the scar. Histologically, dense inflammatory infiltrate and increased vascularity was apparent 1 month after laser sessions and disappeared at 3 months. Thinner better organized collagen bundle could be seen in 3 months after samples. MMP9 was significantly increased in after treatment samples but without significant correlation with VSS. Fractional CO 2 resurfacing is safe but affects mainly pliability of K and HTS with collagen remodeling apparent 3 months after therapy. MMP9 may play a role in mechanism of action of CO 2 laser in K and HTS.

Keloids and hypertrophic scars are caused by cutaneous injury and irritation, including trauma, insect bite, burn, surgery, vaccination, skin piercing, acne, folliculitis, chicken pox, and herpes zoster infection. Notably, superficial injuries that do not reach the reticular dermis never cause keloidal and hypertrophic scarring. This suggests that these pathological scars are due to injury to this skin layer and the subsequent aberrant wound healing therein. The latter is characterized by continuous and histologically localized inflammation. As a result, the reticular layer of keloids and hypertrophic scars contains inflammatory cells, increased numbers of fibroblasts, newly formed blood vessels, and collagen deposits. Moreover, proinflammatory factors, such as interleukin (IL)-1α, IL-1β, IL-6, and tumor necrosis factor-α are upregulated in keloid tissues, which suggests that, in patients with keloids, proinflammatory genes in the skin are sensitive to trauma. This may promote chronic inflammation, which in turn may cause the invasive growth of keloids. In addition, the upregulation of proinflammatory factors in pathological scars suggests that, rather than being skin tumors, keloids and hypertrophic scars are inflammatory disorders of skin, specifically inflammatory disorders of the reticular dermis. Various external and internal post-wounding stimuli may promote reticular inflammation. The nature of these stimuli most likely shapes the characteristics, quantity, and course of keloids and hypertrophic scars. Specifically, it is likely that the intensity, frequency, and duration of these stimuli determine how quickly the scars appear, the direction and speed of growth, and the intensity of symptoms. These proinflammatory stimuli include a variety of local, systemic, and genetic factors. These observations together suggest that the clinical differences between keloids and hypertrophic scars merely reflect differences in the intensity, frequency, and duration of the inflammation of the reticular dermis. At present, physicians cannot (or at least find it very difficult to) control systemic and genetic risk factors of keloids and hypertrophic scars. However, they can use a number of treatment modalities that all, interestingly, act by reducing inflammation. They include corticosteroid injection/tape/ointment, radiotherapy, cryotherapy, compression therapy, stabilization therapy, 5-fluorouracil (5-FU) therapy, and surgical methods that reduce skin tension.

Keloid scars are characterized by the excessive proliferation of fibroblasts and an imbalance between the production and degradation of collagen, leading to its buildup in the dermis. There is no “gold standard” treatment for this condition, and the recurrence is frequent after surgical procedures removal. In vitro studies have demonstrated that photobiomodulation (PBM) using the blue wavelength reduces the proliferation speed and the number of fibroblasts as well as the expression of TGF-β. There are no protocols studied and established for the treatment of keloids with blue LED. Therefore, the purpose of this study is to determine the effects of the combination of PBM with blue light and the intralesional administration of the corticoid triamcinolone hexacetonide on the quality of the remaining scar by Vancouver Scar Scale in the postoperative period of keloid surgery. A randomized, controlled, double-blind, clinical trial will be conducted involving two groups: 1) Sham (n = 29): intralesional administration of corticoid (IAC) and sham PBM in the preoperative and postoperative periods of keloid removal surgery; and 2) active PBM combined with IAC (n = 29) in the preoperative and postoperative periods of keloid removal surgery. Transcutaneous PBM will be performed on the keloid region in the preoperative period and on the remaining scar in the postoperative period using blue LED (470 nm, 400 mW, 4J per point on 10 linear points). The patients will answer two questionnaires: one for the assessment of quality of life (Qualifibro-UNIFESP) and one for the assessment of satisfaction with the scar (PSAQ). The team of five plastic surgeons will answer the Vancouver Scar Scale (VSS). All questionnaires will be administered one, three, six, and twelve months postoperatively. The keloids will be molded in silicone prior to the onset of treatment and prior to excision to assess pre-treatment and post-treatment size. The same will be performed for the remaining scar at one, three, six, and twelve months postoperatively. The removed keloid will be submitted to histopathological analysis for the determination of the quantity of fibroblasts, the organization and distribution of collagen (picrosirius staining), and the genic expression of TGF-β (qPCR). All data will be submitted to statistical analysis. Trial registration: This study is registered in ClinicalTrials.gov (ID: NCT04824612 ).

The skin is the largest organ of the body, which meets the environment most directly. Thus, the skin is vulnerable to various damages, particularly burn injury. Skin wound healing is a serious interaction between cell types, cytokines, mediators, the neurovascular system, and matrix remodeling. Tissue regeneration technology remarkably enhances skin repair via re-epidermalization, epidermal-stromal cell interactions, angiogenesis, and inhabitation of hypertrophic scars and keloids. The success rates of skin healing for burn injuries have significantly increased with the use of various skin substitutes. In this review, we discuss skin replacement with cells, growth factors, scaffolds, or cell-seeded scaffolds for skin tissue reconstruction and also compare the high efficacy and cost-effectiveness of each therapy. We describe the essentials, achievements, and challenges of cell-based therapy in reducing scar formation and improving burn injury treatment.

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. 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. 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. 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. 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. The clinical trial registration number: ChiCTR2000030141. Name of trial registry: Chinese Clinical Trial Registry (http://www.chictr.org.cn/).

Background Consequently, the management of post burn hypertrophic scars and keloid in children are a great challenge for the physicians, parents, and children themselves. Purpose of the Study To assess the efficacy and safety of treating hypertrophic and keloid scars with botulinum toxins injections. Patients and Methods This is a randomized intra‐patient comparative study was conducted on 15 children with post burn hypertrophic and keloid scars. Children were randomized to receive Intralesional injection of botulinum toxins on one part of the hypertrophic scar/keloid where the other part was left as a control. The assessment of clinical improvement was measured by the Vancouver scar scale (VSS) and by skin analysis camera system. Sessions were performed every month for 6 months. Results Clinical and statistical dramatic improvement in the vascularity, pliability, and height of the lesions which have been injected with neuronox. Evaluation of the lesions by the Antera camera has proven marked changes in the vascularity and height. There was no correlations between Vancouver score improvement and variables such as the age, sex, skin type, and duration and lesion type. Conclusions The botulinum toxins proved its efficacy and safety in treatment of hypertrophic scars and keloid in children. It improved the associated itching and pain. Moreover it improves the pliability, erythema, and thickness of the scars.

Keloids are a type of fibrotic disease characterized by excessive collagen production and extracellular matrix (ECM) deposition. The symptoms of pain and itching and frequent recurrence after treatment significantly impact the quality of life and mental health of patients. A deeper understanding of the pathogenesis of keloids is crucial for the development of an effective therapeutic approach. Fibroblasts play a central role in the pathogenesis of keloids by producing large amounts of collagen fibers. Recent evidence indicates that keloids exhibit high immune cell infiltration, and these cells secrete cytokines or growth factors to support keloid fibroblast proliferation. This article provides an update on the knowledge regarding the keloid microenvironment based on recent single-cell sequencing literature. Many inflammatory cells gathered in keloid lesions, such as macrophages, mast cells, and T lymphocytes, indicate that keloids may be an inflammatory skin disease. In this review, we focus on the communication from immune cells to the fibroblasts and the potential of immunotherapy for keloids. We hope that this review will trigger interest in investigating keloids as an inflammatory disease, which may open up new avenues for drug development by targeting immune mediators.