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Keloids and hypertrophic scars are different expressions of the same derailment of wound healing; their biological behaviors and appearances are quite different. The clinical differences between hypertrophic scars and keloids have long been recognized. However, distinguishing between the two types of scars on histology is sometimes difficult as the...
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Context 1
... (66.66%) keloid scars and in (100%) hypertrophic scars. Rare cellularity was a feature of normal scars. Presence of cellularity was correlated only to a small extent with the expression of α-SMA by these cells; positive α-SMA indicates that the cells were myofibroblasts (Table 3). Diffused positive α-SMA was seen only in (33.33%) keloid scars ( Fig. 6: a, b, c), while all hypertrophic scars (100%) failed to show expression of α-SMA (Fig. 7). Collagen in the nodules of hypertrophic scar were generally oriented parallel to each other. Horizontal fibrous bands in the upper reticular dermis were prominent in (93.33%) keloid scars ( Fig. 4) and were absent in all (100%) of the hypertrophic and ...
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A continuum hypothesis-based model is presented for the simulation of the formation and the subsequent regression of hypertrophic scar tissue after dermal wounding. Solely the dermal layer of the skin is modeled explicitly and it is modeled as a heterogeneous, isotropic and compressible neo-Hookean solid. With respect to the constituents of the der...
Objectives
Keloid and hypertrophic scars are abnormal manifestations of wounds that occur following skin injuries in the form of local proliferation of fibroblasts and increased production of collagen. There are several ways to cure these scars; treatment must be selected based on the nature of the scars. In this clinical trial, two methods—cryothe...
Aim: Scar prevention and reduction is an area of therapeutic opportunity and unmet medical need. With no current effective scar therapy, patients are often disappointed in their appearance
post surgery and re-present to surgeons, only to be turned away. The purpose of this study was to develop and test a device that produces intermittent parallel...
Unlabelled:
A chemical burn refers to irritation and destruction of human tissue caused by exposure to a chemical, usually by direct contact with the chemical or its fumes. The study investigated the trend and complications following chemical burns and their management.
Methods:
The study involved a retrospective review of Burns Registry at the...
Introduction
Keloids are hypertrophic scars that commonly arise in the ear region. The authors’ objectives were to (1) evaluate effectiveness of surgical shave excision followed by intralesional triamcinolone acetonide and onabotulinumtoxinA injections; and (2) evaluate safety and patient satisfaction.
Methods and Materials
This study was a retros...
Citations
... The prevalence and high degree of complications that can occur when the integrity of the skin is compromised is one of the major concerns in health care, and it becomes more challenging when chronic wounds are associated with other pathologies that can disrupt the healing process (diabetes mellitus, systemic atherosclerosis or local ischemia and pressure ulcers) [1][2][3][4][5][6]. In general, all wounds tend to be chronic and are characterized by prolonged inflammation and senescent, immature or highly differentiated fibroblasts that respond ineffectively to the stimulation of the cytokines involved in the healing process [7][8][9][10][11][12][13]. In response to injury, histamines, free radicals and inflammatory cytokines are released, and they amplify vasodilatory processes and tissue edema [12,[14][15][16][17], promoting the penetration of inflammatory cells into the wound site, activating the cascade of events which leads to the elimination of cellular and tissue debris, releasing growth factors and initiating the reorganization of the extracellular matrix [18][19][20] by activating metalloproteinases that affect the intercellular matrix, arresting the wound at the inflammatory stage [18][19][20][21][22]. ...
Currently, the treatment of wounds is still a challenge for healthcare professionals due to high complication incidences and social impacts, and the development of biocompatible and efficient medicines remains a goal. In this regard, mesoporous materials loaded with bioactive compounds from natural extracts have a high potential for wound treatment due to their nontoxicity, high loading capacity and slow drug release. MCM-41-type mesoporous material was synthesized by using sodium trisilicate as a silica source at room temperature and normal pressure. The synthesized mesoporous silica was characterized by using Scanning Electron Microscopy (SEM), Transmission Electron Microscopy (TEM), N2 absorption–desorption (BET), Dynamic Light Scattering (DLS) and Fourier transform infrared spectroscopy (FT-IR), revealing a high surface area (BET, 1244 m2/g); pore diameter of approx. 2 nm; and a homogenous, ordered and hexagonal geometry (TEM images). Qualitative monitoring of the desorption degree of the Salvia officinalis (SO) extract, rich in ursolic acid and oleanolic acid, and Calendula officinalis (CO) extract, rich in polyphenols and flavones, was performed via the continuous recording of the UV-VIS spectra at predetermined intervals. The active ingredients in the new composite MCM-41/sage and marigold (MCM-41/SO&CO) were quantified by using HPLC-DAD and LC-MS-MS techniques. The evaluation of the biological composites’ activity on the wound site was performed on two cell lines, HS27 and HaCaT, naturally involved in tissue-regeneration processes. The experimental results revealed the ability to stimulate collagen biosynthesis, the enzymatic activity of the main metalloproteinases (MMP-2 and MMP-9) involved in tissue remodeling processes and the migration rate in the wound site, thus providing insights into the re-epithelializing properties of mesoporous composites.
... Keloid formation is due to the imbalance of the mast cells in the inflammatory cell population. 9 Electron microscopic studies showed welldeveloped, rough endoplasmic reticulum in keloid fibroblasts. The collagen fibrils are banded into thick fibres separated by amorphous material which is not seen hypertrophic scars. ...
Keloids are benign fibroproliferative growth seen on the skin usually secondary to trauma. They are scar tissues that project above the skin surface and may be tender or pruritic. They cause functional and aesthetic discomfort to the patient. This is a case report of a 34 year old woman who was diagnosed as a case of keloid of the left auricle and treated surgically. Keloids have a high degree of recurrence even after treatment. It is crucial to differentiate keloids from hypertrophic scars and treat them accordingly.
Objective: To determine the frequency and antibiotic susceptibility of bacteria isolated in patients with blepharitis. StudyDesign: Cross-sectional study. Place and Duration of Study: Armed Forces Institute of Ophthalmology, Rawalpindi Pakistan, from Oct 2019 to Oct 2021. Methdology: 160 cases of blepharitis, during a period of 2 years, who were not using topical or systemic antibiotics were recruited in this cross-sectional study. After detailed history and slit-lamp examination of eyelids and tears film each patient underwent sample collection under aseptic conditions, from the eyelid margin. The samples were inoculated in a culture of blood agar and chocolate agar (Biomeriux) , Then the susceptibility of the identified bacteria to common systemic and topical antibiotics were tested using the disc diffusion method (Rosco Neo-Sensitab). Results: In 160 patients,118(73.7%) were males and 42(26.3%) were females. According to type of blepharitis, 98(61.3%) had posterior blepharitis and 62(38.7%) had anterior blepharitis.Culture of eyelid sample of 77(48.1%) patients showed growth of coagulase-negative staphylococcus Coagulase-negative staphylococcus (CoNS) show greater resistance towards Penicillin 77(100%), Ciprofloxacin 55(72.5%) and Erythromycin 33(42.8%) however more susceptibility was shown towards Linezolid (CoNS). 71(45%) had Staphylococcus aureus isolated from their culture. 77(100%),Vancomycin 77(100%), Gentamycin 66(85.8%), Chloramphenicol 56(74.5%) and Cotrimoxazole 55(72.5%).Staphylococcus aureus show greater resistance towards Penicillin 72(100%),Ciprofloxacin 41(56.9%) and Tetracyclins 30(41.6%) however more susceptibility was found towards Gentamycin 72(100%), Linezolid 72(100%),Vancomycin 72(100%) and Chloramphenicol 61(84.7%). Conclusion: Coagulase-negative staphylococcus (CoNS) and Staphylococcus aureus have been the main isolated organisms in blepharitis. These bacteria have been shown to be resistant to Penicillin
For many decades, in the literature there has been a discussion about the role of skin scars in the development of tumors. Despite this, the distinctive features of their formation and pathogenetic mechanisms remain not fully revealed. The princ-i ples of malignant tumors’ development of healthy and pathologically altered skin remain unresolved. There are conflicting data on the influence of climatogeographic and social factors on the development of skin cancer. It has been established that ultraviolet irradiation plays an important role in the development of malignant skin neoplasms. Intensive insolation is the cause of the development of pathological changes in the skin and vascular tissue. Perhaps one of the probable patho-genic factors is the influence of damaging doses of solar energy. On the skin structure in Central Asian countries, where skin cancer occupies the leading rank among all malignant tumors. The results of treatment in skin cancer that has developed in the area of scarring of various origins – mechanical, traumatic injuries, or chemical, thermal burns – remain disappointing. The development of relapses and metastases in the nearby anatomic structures after treatment worsen the quality of life in the patients; dictate the selection of adequate methodological approaches to this group of patients.
Fibrosis is a condition characterized by thickening or/and scarring of various tissues. Fibrosis may develop in almost all tissues and organs, and it may be one of the leading causes of morbidity and mortality. It provokes excessive scarring that excels the usual wound healing response to trauma in numerous organs. Currently, very little can be done to prevent tissue fibrosis, and it is almost impossible to reverse it. Anti-inflammatory and immunosuppressive drugs are among the few treatments that may be efficient in preventing fibrosis. Numerous publications suggest that cannabinoids and extracts of Cannabis sativa have potent anti-inflammatory and anti-fibrogenic properties. In this review, we describe the types and mechanisms of fibrosis in various tissues and discuss various strategies for prevention and dealing with tissue fibrosis. We further introduce cannabinoids and their potential for the prevention and treatment of fibrosis, and therefore for extending healthy lifespan.
Although hypertrophic scars and keloidsboth generate excessive scar tissue, keloids are characterized by their extensive growth beyond the borders of the original wound, which is not observed in hypertrophic scars. Whether or not hypertrophic scars and keloids are two sides of the same coin or in fact distinct entities, remains a topic of much debate. However, proper comparison between the two ideally occurs within the same study, but this is the exception rather than the rule. For this reason, the goal of this review was to summarize and evaluate all publications in which both hypertrophic scars and keloids were studied and compared to one anotherwithin the same study. The presence of horizontal growth is the mainstay of the keloid diagnosis and remains the strongest argument in support of keloids and hypertrophic scars being distinct entities, the histopathological distinction is less straightforward. Keloidal collagen remains the strongest keloid parameter, but dermal nodules and α‐SMA‐immunoreactivity are not limited to hypertrophic scars alone. Ultimately, the current hypertrophic scars – keloid differences are mostly quantitative in nature rather than qualitative, and many similar abnormalities exist in both lesions. Nonetheless, the presence of similarities does not equate the absence of fundamental differences, some of which may not yet have been uncovered given how much we still have to learn about the processes involved in normal wound healing. It therefore seems pertinent to continue treating hypertrophic scars and keloids as separate entities, until such a time as new findings more decisively convinces us otherwise.
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 in vivo and in vitro 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 in vitro 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.
Scar research is challenging because rodents do not naturally form excessive scars, and burn depth, size, and location cannot be controlled in human longitudinal studies. The female, red Duroc pig model has been shown to form robust scars with biological and anatomical similarities to human hypertrophic scars. To more closely mimic the mode of injury, recreate the complex chemical milieu of the burn wound environment and enhance scar development, an animal model of excessive burn-induced scarring was developed and compared with the more commonly used model, which involves excisional wounds created via dermatome. Standardized, full-thickness thermal wounds were created on the dorsum of female, red Duroc pigs. Wounds for the dermatome model were recreated using two different total dermatome settings: ∼1.5 mm and ≥ 1.9 mm. Results from analysis over 150 days showed that burn wounds healed at much slower rate and contracted more significantly than dermatome wounds of both settings. The burn scars were hairless, had mixed pigmentation, and displayed four-fold and two-fold greater excess erythema values, respectively, compared with ∼1.5 mm and ≥ 1.9 mm deep dermatome injuries. Burn scars were less elastic, less pliably and weaker than scars resulting from excisional injuries. Decorin and versican gene expression levels were elevated in the burn group at day 150 compared with both dermatome groups. In addition, transforming growth factor-beta 1 was significantly up-regulated in the burn group versus the ∼1.5 mm deep dermatome group at all time points, and expression remained significantly elevated versus both dermatome groups at day 150. Compared with scars from dermatome wounds, the burn scar model described here demonstrates greater similarity to human hypertrophic scar. Thus, this burn scar model may provide an improved platform for studying the pathophysiology of burn-related hypertrophic scarring, investigating current anti-scar therapies, and development of new strategies with greater clinical benefit. This article is protected by copyright. All rights reserved.
Background:
The pathogenesis underlying keloid formation is still poorly understood. Research has focused mostly on dermal abnormalities, while the epidermis has not yet been studied.
Objectives:
To identify differences within the epidermis of mature keloid scars compared with normal skin and mature normotrophic and hypertrophic scars.
Methods:
Rete ridge formation and epidermal thickness were evaluated in tissue sections. Epidermal proliferation was assessed using immunohistochemistry (Ki67, keratins 6, 16 and 17) and with an in vitro proliferation assay. Epidermal differentiation was evaluated using immunohistochemistry (keratin 10, involucrin, loricrin, filaggrin, SPRR2, SKALP), reverse-transcriptase polymerase chain reaction (involucrin) and transmission electron microscopy (stratum corneum).
Results:
All scars showed flattening of the epidermis. A trend of increasing epidermal thickness correlating to increasing scar abnormality was observed when comparing normal skin, normotrophic scars, hypertrophic scars and keloids. No difference in epidermal proliferation was observed. Only the early differentiation marker involucrin showed abnormal expression in scars. Involucrin was restricted to the granular layer in healthy skin, but showed panepidermal expression in keloids. Normotrophic scars expressed involucrin in the granular and upper spinous layers, while hypertrophic scars resembled normotrophic scars or keloids. Abnormal differentiation was associated with ultrastructural disorganization of the stratum corneum in keloids compared with normal skin.
Conclusions:
Keloids showed increased epidermal thickness compared with normal skin and normotrophic and hypertrophic scars. This was not due to hyperproliferation, but possibly caused by abnormal early terminal differentiation, which affects stratum corneum formation. Our findings indicate that the epidermis is associated with keloid pathogenesis and identify involucrin as a potential diagnostic marker for abnormal scarring.
