Abnormally Raised Or Thickened Scar
Clinics (Sao Paulo). 2014 Aug; 69(8): 565–573.
Update on hypertrophic scar treatment
Felipe Bettini Rabello
IUniversidade de São Paulo, Faculdade de Medicina de Ribeirão Preto, Ribeirão Preto/SP, Brazil.
Cleyton Dias Souza
IiUniversidade de São Paulo, Faculdade de Medicina de Ribeirão Preto, Programa de Pós-Graduação da Clinica Cirúrgica, Ribeirão Preto/SP, Brazil.
Jayme Adriano Farina Júnior
IIIUniversidade de São Paulo, Hospital das Clínicas da Faculdade de Medicina de Ribeirão Preto, Departamento de Cirurgia e Anatomia, Divisão de Cirurgia Plástica, Ribeirão Preto/SP, Brazil.
Received 2013 Sep 13; Revised 2013 Dec 2; Accepted 2014 Feb x.
Abstract
Scar formation is a event of the wound healing process that occurs when body tissues are damaged by a physical injury. Hypertrophic scars and keloids are pathological scars resulting from abnormal responses to trauma and tin can exist itchy and painful, causing serious functional and cosmetic disability. The current review will focus on the definition of hypertrophic scars, distinguishing them from keloids and on the various methods for treating hypertrophic scarring that have been described in the literature, including treatments with clearly proven efficiency and therapies with doubtful benefits. Numerous methods accept been described for the handling of aberrant scars, but to date, the optimal treatment method has not been established. This review will explore the differences betwixt dissimilar types of nonsurgical management of hypertrophic scars, focusing on the indications, uses, mechanisms of action, associations and efficacies of the following therapies: silicone, pressure garments, onion extract, intralesional corticoid injections and bleomycin.
Keywords: Hypertrophic Scar, Review, Pathological Scars, Update
INTRODUCTION
Hypertrophic scars (HTSs) are divers equally visible and elevated scars that do non spread into surrounding tissues and that often regress spontaneously (i). These scars are characterized by proliferation of the dermal tissue, with excessive degradation of fibroblast-derived extracellular matrix (ECM) proteins and especially collagen, over long periods and by persistent inflammation and fibrosis (two).
Numerous methods accept been described for the treatment of abnormal scars, simply to date, the optimal treatment method has not been established. A wide diversity of treatments accept been advocated for HTSs. Among these treatments are surgical excision with or without grafting (1), pressure therapy (3), intralesional interferon (4), topical and intralesional corticosteroids (five), intralesional bleomycin (6), laser therapy (7), silicone gel sheeting (8), onion extract gel and other therapies directed at collagen synthesis (9).
Distinguishing hypertrophic scars from keloids
When faced with patients seeking treatment for pathological scars, many physicians have difficulty in differentiating HTSs from keloids; therefore, it is crucial to establish criteria to distinguish them.
HTSs are usually raised, although rarely elevated more than than 4 mm above the skin; red or pink in color; difficult; and pruritic. Additionally, these scars practise non extend across the general geographic margins of the wound and tend to regress over time (x) (Figure 1). HTSs primarily incorporate type 3 collagen, oriented parallel to the epidermal surface and with abundant nodules and large extracellular collagen filaments (xi).
Hypertrophic scar regression in a burned child after four years (A and B). Hypertrophic scars are usually raised, although rarely elevated more than 4 mm to a higher place the skin; red or pink in color; difficult; and pruritic. Additionally, these scars do not extend across the general geographic margins of the wound and tend to regress over time.
In contrast, keloids continue to evolve over time, without a quiescent or regressive stage and practice infiltrate the surrounding tissue (Figure ii). Keloids appear every bit firm, mildly tender, bosselated tumors with a shiny surface and occasional telangiectasia. The epithelium is thinned and there may be focal areas of ulceration. The color is pink to royal and may be accompanied past hyperpigmentation (12). The initial lesions are erythematous and become brownish red, followed by paling as they age. The lesions preferentially develop on the earlobes, shoulders and presternal skin; are void of pilus follicles and other glands; and usually projection higher up the level of the surrounding skin (thirteen). Keloids are primarily composed of abnormally thick, irregularly branched and septal disorganized type I and Iii collagen bundles without nodules and with backlog myofibroblasts (11) and overproduction of multiple fibroblast proteins, indicating the persistence of wound healing or even a failure to downregulate wound-healing cells. In add-on, keloids are not triggered to enter the terminal phase of wound healing, or the "remodeling" phase, whereas HTSs will somewhen practise so (xiv).
Keloid evolution subsequently seven years (A and B). Keloids continue to evolve over time, without a quiescent or regressive phase, and infiltrate the surrounding tissue.
Distinguishing HTSs from keloids histopathologically is occasionally difficult considering thickened hyalinized collagen (keloidal collagen), the hallmark of keloids, is not e'er detectable and considering α-polish muscle actin (α-SMA), a differentiating marker of HTSs, is variably expressed in both types of scars (15).
The histopathological findings most unremarkably observed in HTSs are flattening of the epidermis and replacement of the papillary and reticular dermis by scar tissue with prominent vertically oriented blood vessels (Figure iii). In keloids, there is no flattening of the overlying epidermis, no scarring of the papillary dermis, the presence of a significant corporeality of keloidal collagen, an absence of prominent vertically oriented blood vessels and the presence of a significant disarray of fibrocollagenous fascicles (Figure iv) (15).
The histology of hypertrophic scars is characterized by replacement of the papillary and reticular dermis by scar tissue with prominent vertically oriented claret vessels. The fibrous bundles are parallel and horizontal in the upper dermis. (Masson's trichrome, 100X).
The histology of keloids is characterized past well-demarcated and disorganized gristly tissue unremarkably involving the upper half or two-thirds of the dermis. The collagen fibers are noticeably thicker (Masson's trichrome, 100X).
Differential and exclusive diagnosis
The differential and exclusive diagnosis of diseases that are similar to keloids and HTSs is of import because various types of cancerous tumors resemble these scars (16)–(19). For example, malignant dermatofibrosarcoma protuberans (DFSP) tumors have been mistaken for keloids or HTSs (xvi,17).
Nodular scleroderma and keloidal scleroderma are rare benign tumors with lesions that clinically resemble keloids (20). The pare lesions are characteristically nodules or plaques, difficult in consistency, and nontender, with a predilection for the superior portions of the thorax and sparing of the face and hands (21).
Gonzalez-Vela et al. (22) described keloids and HTSs as differential diagnoses of sclerotic neurofibroma. Sclerotic neurofibroma is differentiated from a keloid past an absence of previous surgical excision and by the positivity of the sclerotic neurofibroma cells for the protein S100 (22).
Other rare, benign keloid and HTS-similar diseases include keloidal granuloma (23), erythema elevatum diutinum (24), infantile digital fibromatosis (25), dermatofibroma,(26) penile edema (27), pseudoangiomatous hyperplasia (28) and lichen sclerosus (29).
Pilus folliculitis occasionally leads to hypertrophic scarring (30) but more than often leads to progressive folliculitis caused by bacterial or fungal infection. The nape is an area of predilection for hair folliculitis. Treatment of any infection should exist main and steroid injection is contraindicated for infection. Moreover, a fungus may cause a peel nodule that mimics a keloid (31). Thus, examination for fungal infection should be conducted in cases of nape hair folliculitis, even if the nodule appears to exist a keloid or HTS.
In conclusion, the following issues are considered important in the examination of a keloid or HTS: a biopsy should be conducted in anomalous cases because malignant affliction may be the original or secondary problem, steroid injection should be performed simply subsequently careful consideration because malignancy or infections may be present, making a careful differential diagnosis is peculiarly challenging in African-Americans because the skin and the tumor colors are often similar and the presence of bacterial or fungal infection should be investigated (32).
Demographics
The majority of individuals who develop HTSs and keloids are immature, with ages ranging from 10 to 30 years old. The elderly rarely develop these lesions (33). This observation is partly attributed to the post-obit facts: young individuals are more prone to trauma; their skin mostly possesses more elastic fibers, resulting in greater tension; and the rate of collagen synthesis is greater in younger individuals (34). Keloids are more common in patients with darker peel, with an incidence of 4.v% to 16% in the blackness and Hispanic populations (34).
HTSs are a mutual complexity of fire injury. In the adult world, approximately four million patients acquire scars due to burns each year and the incidence is even greater in developing countries (4). Previous studies take reported diverging incidences of hypertrophic scarring, with incidence rates varying from 40% to 94% following surgery and from 30% to 91% following burns (35,36).
Etiology
Wound healing is classically divided into iv stages: hemostasis, inflammation, proliferation and tissue remodeling. In these four stages, at that place are complicated interactions within a complex network of profibrotic and antifibrotic molecules, such as growth factors, proteolytic enzymes and ECM proteins (37). Each molecule has its ain role in the unlike phases of the wound healing procedure. As soon as an injury occurs, the process of hemostasis begins and the bleeding is controlled by the assemblage of platelets at the site of injury. The subsequent germination of a fibrin clot helps to stop the bleeding and provides a scaffold for the attachment and proliferation of cells. Growth factors and cytokines are mainly secreted past inflammatory cells and contribute to the initiation of the proliferative phase of wound healing. Later, angiogenesis and collagen synthesis, followed by tissue remodeling complete the stages of the wound healing process.
The delicate balance of the deposition and degradation of ECM proteins is disrupted when either excessive production of collagen, proteoglycans and fibronectin past fibroblasts or scarce degradation and remodeling of the ECM occur (38). HTSs occur when the inflammatory response to injury is prolonged, leading to the pathological characteristics of HTSs, including increased vascularization, hypercellularity, excessive collagen degradation and a subtract in small leucine-rich proteoglycans (SLRPs) (39,40).
HTS tissue contains enhanced amounts of fibroblasts that exhibit an altered phenotype and higher expression of transforming growth cistron beta-ane (TGF-β1) than normal fibroblasts practise (41). An increase in or prolonged activity of TGF-β1 leads to overproduction and excess deposition of collagen by fibroblasts, often resulting in HTS germination (42). Fibroblasts in HTSs may differentiate into myofibroblasts and account for increased ECM synthesis and contraction of tissue. These cells have a particular phenotype that differs from that of fibroblasts based on their expression of α-SMA (43). Myofibroblasts in HTSs are less sensitive to apoptotic signals, coupled with an ability to produce more collagen and play an important role in HTS formation (43).
Clinical manifestations
The clinical manifestations of HTSs are variable and correlate with a variety of causes that initiate HTS germination. HTSs can develop anywhere on the body. In contrast, keloids preferentially develop on the earlobes, shoulders and presternal skin; are void of hair follicles and other glands; and commonly projection above the level of the surrounding skin (thirteen). Curiously, pathological scars are rare on the scalp. Farina Jr et al. recently described a casuistic study of 413 surgical procedures involving collection of thin peel grafts from the scalp, without evolution of HTSs or keloids among 295 cases over a period of ten years (44).
Hypertrophic scarring following surgical procedures, trauma and especially burns is a significant concern for patients and a challenging trouble for clinicians because information technology can exist painful, pruritic, erythematous, raised and cosmetically unacceptable. A previous report reported that the most common and pitiful complications in fire patients who developed HTSs were aberrant appearance (75.ii%), pruritus (73.three%) and pain (67.6%) (45). The crusade of pruritus in HTSs and keloid scars is not yet well characterized, but recent studies have indicated the probable involvement of direct activation of opioid receptors identified in the skin (46).
Prevention and non-surgical treatment
At that place is bear witness suggesting that increased mechanical tension can initiate HTS formation (47). Based on this hypothesis, it makes sense to minimize mechanical forces later surgery. Surgical excision scars should be positioned forth, rather than beyond, relaxed skin tension lines whenever possible. An appropriate strength, depth and number of sutures should ensure that the gamble of dehiscence is minimized.
Inflammation is also known to contribute to hypertrophic scarring, (49) and every attempt to minimize the inflammatory response should be fabricated by ascertaining clean surgery and adept wound care to foreclose infection thereafter. Using inert suture materials is also important in this context (48).
In patient candidates for skin grafts, the donor site must be well chosen by the surgeon in consultation with the patient to try to hide or avoid HTSs or keloids. In burn patients, the corresponding writer believes that using the scalp as a source of thin skin grafts tin reduce the level of visible artful deformities at donor sites in patients who have already suffered the immense trauma that being a burn victim entails.
Conceptually and practically, handling and prevention regimens can be similar and the following section presents the clinical data for both. Early diagnosis tin can considerably affect the outcome. At that place is testify that the most successful non-surgical treatment of an HTS or keloid is achieved when the scar is immature and the overlying epithelium is intact, although further studies are necessary to ostend this concept (50).
Silicone
Silicone gel sheeting (SGS) has been widely used in clinical practice for the treatment of HTSs since the early on 1980s. There is good evidence of the efficacy of the SGS, which has become standard practice among plastic surgeons (51).
Although gel sheeting is effective for HTS handling, patient compliance may not be satisfactory for the following reasons: skin reaction to the record used for fixation; excessive sweating; difficulty in its application; and the visibility of the treatment in the instance of scars located in visible areas, such as the face up (52).
In contrast, silicone gel does not require fixation and is nearly invisible when dry, suggesting that it could be peculiarly useful in visible areas (52). However, there are certain problems in its awarding. For example, silicone gel requires multiple applications in a day and one must wait long plenty for drying considering the dressing may be smudged. Friction by clothes may too contribute to early removal of the silicone motion-picture show (51). Because of these problems, silicone gel use may not always be practical.
Karagoz et al. constitute no statistically pregnant difference betwixt silicone gel and silicone gel sheet groups when their scores on the Vancouver Scar Scale after handling were compared. This finding suggests that silicone gel is virtually likely as effective equally SGS for the handling of HTSs (52).
The machinery of activity of topical silicone materials in the treatment of HTSs is not well understood and various mechanisms of activeness have been proposed. It has been suggested that the materials' therapeutic effect is not due to force per unit area, simply rather to decreased scarring via wound hydration. In that location is testify that SGS affects the hydration status of the scar by decreasing the water vapor transmission rate to nearly half that of normal peel, causing a buildup of moisture on the skin surface under the silicone sheet (53). This bear witness suggests that the stratum corneum acts as a water reservoir, with fluid accumulating below the gel, although when visualized directly, this miracle is non evident (54). Hydration and occlusion therefore seem to be the principal modes of SGS activeness and increased peel hydration is about probable responsible for decreased capillary activity, reduced hyperemia and reduced collagen deposition (55). Furthermore, altered hydration is idea to crusade electrostatic changes that influence collagen deposition and remodeling within the scar (56). The static electricity generated by friction has also been proposed as a plausible reason for silicone'due south anti-scarring furnishings (57).
The lower water vapor transmission charge per unit and the aggregating of water below the material can cause skin maceration (58). Other mutual side effects associated with gel sheeting include persistent pruritus, skin breakup, skin rash, foul smell from the gel, poor durability of the sheet, failure of the sheet to improve the hydration of dry scars, a poor response of the scar to treatment and poor patient compliance (59,threescore). Like to pressure therapy, detailed multimedia-based patient instruction improves compliance with SGS, resulting in a meliorate scar upshot (threescore). Obviously, the key to the success of this therapy is to ensure that hygienic precautions are taken, particularly when it is used in combination with pressure in children or in warm atmospheric condition or climates (60). Information technology must exist noted, however, that complications increase with the use of combined pressure and SGS therapy (60).
Applying silicone gel twice daily or wearing SGS 12 to 24 h per twenty-four hours for half dozen to 12 months, with temporary interruption when adverse furnishings appear, is recommended (61).
Pressure garments
Using mechanical compressive strength exerted by pressure level garments to treat HTSs in burn patients was first described in 1860 (62). It was only in the 1960s that this handling became standard in several burn centers to accelerate the remodeling phase of wound healing (62). Prophylactic pressure level is recommended in burn patients if spontaneous closure of the wound takes longer than ten to 14 days and in those requiring grafting (2).
Currently, elastic pinch using rubberband garments is the predominant means of both prophylaxis and treatment for HTSs (63), despite controversial show-based data about their value in reducing the prevalence or magnitude of scarring (63). In fact, studies investigating force per unit area garments take found no meaning difference between treatments involving the use of loftier-force per unit area garments, lower-pressure level garments, or no pressure level at all (64). Others, however, claim that pressure therapy achieves HTS regression success rates of threescore% to 85% (63), without any conclusive evidence.
To date, the working mechanism of pressure and the way that pressure positively influences the development and maturation of HTSs are not fully understood and explanations remain hypothetical. However, many studies have been performed to try to explicate the possible mechanisms of action, exploring theories based on hypoxia, biochemical changes, and cellular and collagenous influences. Sure valuable evidence suggests that force per unit area controls collagen synthesis past limiting the supply of blood, oxygen, and nutrients to the scar tissue (65); reduces collagen production to the levels found in normal scar tissue more rapidly than the natural maturation process does; encourages the realignment of collagen bundles that are already present (66); partly restores the ECM organization observed in normal scarring; and induces the disappearance of fibrogenic α-SMA-expressing myofibroblasts and vascular cells, most likely by apoptosis (67).
Additionally, certain studies have demonstrated that mechanical pinch directly modulates the remodeling stage of wound healing, altering the release and activity of matrix metalloproteinase (MMP)-28 in HTSs and inducing a significant reduction in the poly peptide's presence in keratinocytes in HTSs (68). Moreover, information technology has been suggested that pressure acts by accelerating the remission stage of the postburn reparative process (66).
Currently, the recommendations for the clinical use of pressure garments are restricted to deep dermal wounds that have healed spontaneously over weeks, grafted wounds surrounded by a deep dermal wound that was permitted to heal spontaneously over weeks, wounds in children and immature adults, wounds in individuals with dark pare and wounds in body locations where compression tin exist applied (69). The amount of effective pressure level generated by a given pressure garment is as well still unknown and remains controversial (70). Bug with pressure loss from the garments over time and problems with the compliance of the patients using the garments are nevertheless other factors complicating the outcome (69,70).
Onion extract and heparin gel
Onion extract possesses fibroblast-inhibiting properties that reduce both fibroproliferative activity and the product of ECM, increasing the expression of MMP-1 (71). Heparin strongly interacts with collagen molecules, inducing the formation of the thicker fibrils typical of a mature tissue and too promoting intermolecular bonding in collagen (72). Therefore, heparin and onion extract affect scar development via their inhibitory furnishings on inflammatory processes, fibroblast proliferation and the synthesizing capacity of fibroblasts (72). Onion extract and heparin exert similar antiproliferative effects that depress fibroblast proliferation and reduce scar size in the case of excessive scar formation in HTSs and keloid scars (73).
The topical gel training includes 10% aqueous onion extract, 50 U heparin per gram of gel, and i% allantoin gel, and this conception has been used for many years to treat wounds. Despite the gel's popularity, information demonstrating its efficacy are lacking. Sure clinical studies of the efficacy and tolerability of this topical training have been conducted. Ho et al. constitute onion extract, heparin and allantoin gel to be constructive, condom and elementary to apply for the prevention of scarring in 120 Chinese patients undergoing light amplification by stimulated emission of radiation removal of tattoos. The researchers found that the topical gel preparation reduced the take a chance of scarring significantly, from 23.5% to eleven.v% (72). Willital and Heine studied the effect of the same topical gel preparation on fresh scars after thoracic surgery in children and adolescents. The authors randomly assigned 45 young patients with fresh scars after thoracic surgery to the treatment and institute that the scars in the treated grouping were narrower than those in the untreated group after one year of the treatment (74). In this written report, the benefit of the gel for the treatment of physiologic scars as well as for the treatment of HTSs and keloid scars were described. In a more recent study, the early utilize of onion extract gel in surgical scars resulted in the improvement of scar peak and symptoms, just in that location was no statistically significant difference in the scars' redness, pliability or overall corrective appearance (75). All the same, we have observed that many patients who use a topical grooming containing onion excerpt, heparin and allantoin gel or another onion extract gel do not detect any pregnant improvement in their HTSs.
Intralesional corticosteroid injections
Intralesional corticosteroid injections, used for the treatment of pathological scars since the mid-1960s, continue to play a major role in the regression of HTSs and keloids (76). Steroid injections have been shown to cause HTS and keloid regression in vivo, mainly by decreasing collagen and glycosaminoglycan synthesis, by reducing the inflammatory procedure in the wound, by decreasing fibroblast proliferation and past increasing hypoxia (77). Insoluble triamcinolone acetonide (TAC; 10 to 40 mg/ml), the most common corticosteroid used for the treatment of scars, may exist administered alone or in combination with lidocaine to reduce the pain associated with the injection and several treatments administered one time or twice per month are usually required to attain the desired results (78).
Despite few randomized, prospective studies, there is broad consensus that injected TAC is efficacious and information technology is the first-line therapy for the treatment of keloids and the 2nd-line therapy for the treatment of HTSs if other, easier treatments have not been efficacious. Response rates vary from 50% to 100%, with a recurrence rate of 9% to 50% (73).
Manuskiatti and Fitzpatrick found clinical improvement of HTSs and keloid scars afterwards treatment with an intralesional injection of TAC combined with Contractubex® gel, which appears to be superior to intralesional TAC administered alone in the treatment of keloids and HTSs, with no significant side effects (78).
Although the use of corticosteroids to suppress abnormal scar formation has been relatively effective for most patients, it has also been a troublesome therapy. Intralesional corticosteroid injection is associated with significant injection pain, even using standard doses of triamcinolone (forty mg/ml), with up to 63% of patients experiencing certain side effects, including hypopigmentation, skin and subcutaneous fat atrophy, telangiectasias, rebound furnishings and ineffectiveness (79). Afterward intralesional injection, linear hypopigmentation besides may develop secondary to lymphogenous uptake of the corticosteroid crystals (80).
Bleomycin
Bleomycin sulfate was introduced by Bodokh and Brun in 1996 equally an alternative therapy for keloids and HTSs, based on its activity as an inhibitor of the synthesis of deoxyribonucleic acid (Dna) (81). Bleomycin is a secondary metabolite of a strain of Streptomyces obtained from soil and has antitumor, antiviral and antibacterial action. This compound acts past binding to Dna, whether double stranded and single stranded, causing strand scissions (82). The utilise of intralesional bleomycin has been documented for the treatment of keloids and HTSs, with promising results (83). Certain studies have investigated the furnishings of intradermal bleomycin administration into the skin of healthy individuals (84). From a histologic point of view, bleomycin has been found to cause necrosis of keratinocytes and this handling can as well induce inflammatory infiltration, along with expression of various adhesion molecules (84). Furthermore, the presence of apoptotic cells has been noted in common warts treated with bleomycin (85). Despite these findings, the exact mechanism by which bleomycin induces keloid and HTS regression is non entirely clear.
Apropos the side furnishings of intralesional assistants of bleomycin, hyperpigmentation and dermal cloudburst have developed in the healthy skin surrounding the lesion in only a few cases (86). The systemic side furnishings of bleomycin with intradermal/intralesional administration lonely are not of business concern because the concentration and dosage are not sufficient to incite systemic problems such as hepatotoxicity and pulmonary fibrosis (87).
Certain findings have revealed that bleomycin not just improves cosmetic advent but also relieves patients' pruritus and pain, symptoms often associated with pathological scars. Although intralesional bleomycin is a promising treatment option for keloids and HTSs, further investigation and efficacy trials are needed earlier this agent can exist included in futurity handling protocols (88).
Emerging alternative treatments
The use of interferon alpha, beta and gamma increases collagen lysis. In item, blastoff and gamma inhibit the synthesis of collagen types I and III, acting on mRNA in the cell and reducing the levels of TGF-β. However, interferon application is very painful and it is a plush drug (88).
The drug 5-fluorouracil may exist used alone or in combination with corticosteroid injections and achieves better results when combined with triamcinolone because monotherapy has limited use due to hurting on application (50). The use of a carbon dioxide light amplification by stimulated emission of radiation and an argon laser is ineffective due to recurrences, which are treated with steroids. Intense pulsed lite therapy has shown satisfactory results, although further studies are needed, especially with later on cess of cases (50).
Drugs such as imiquimod, flurandrenolide, clobetasol, tacrolimus, methotrexate and pentoxifylline are several of the tested agents that have shown a clinical response, an increase in the local production of interferon in particular. However, the results must be considered with skepticism until further studies are conducted (89).
Cryotherapy with liquid nitrogen combined with corticosteroids showed a satisfactory response in the handling of keloid scars, although its employ in HTSs has non been assessed (90).
Botulinum toxin type A stimulates collagen germination and hyperbaric oxygen provides pure oxygen at a pressure slightly higher than atmospheric pressure level, leading to decreased growth of atypical fibroblasts and restoration of tissue regeneration. In both cases, use of the treatment does not occur in isolation simply rather every bit a complementary therapy. Still, further studies are necessary (91,92).
Dermal radiofrequency can be another therapeutic option for the treatment of HTSs. This treatment'due south mechanism of activeness is based on a slight increase in the temperature of the skin, increasing the extensibility and reducing the density of collagen (by a lifting effect due to the radio frequency) (93).
Surgery
HTSs quickly increase in size for three to 6 months. And then, after a static stage, they begin to backslide. The scars mature during a period of at least i yr and tin can prove decreased contractures, forth with flattening, softening and repigmentation without whatsoever physical manipulation. For this reason, surgery is commonly not necessary. Nevertheless, surgery is indicated for those cases of HTSs with scar contractures (and particularly joint contractures) that could effect in loss of part (fifty).
HTSs may impair motility when they cantankerous joints or exert abnormal forces on surrounding tissues. The shoulder, elbow, and knee are the most mutual joints affected by contractures subsequently burn down injury (94). Certain fire scars can cause enough impairment of function to require surgical intervention. The techniques of releasing burn scar contractures vary significantly, depending on the individual characteristics of the scar in question. In general, local, linear or small planar scars that impair movement may be lengthened by Z or Five-Y plasty procedures and skin grafts may be necessary later on major contracture release (94). Additionally, the use of a dermal matrix and negative pressure therapy to generate higher-quality skin grafts for the handling of sequelae and contractures in burns is more and more than mutual (95).
Mental status
It is important to investigate a patient'southward current mental condition to exclude the possibility of any psychiatric disorder before initiating treatment planning. Patients presenting a history of severe sadness or other depressive symptoms should be diagnosed and followed past a psychologist and psychiatrist and should start treatment but afterwards discharge by the expert. Psychological stress also seems to be related to the recurrence of fibroproliferative scarring (96).
Patients who are dissatisfied with the treatment of their HTSs often cite a pre-existing psychopathological condition in lawsuits filed against their doctors, claiming that they did not have the mental faculties to sympathise the outcomes and limitations of the proposed treatment. Information technology is necessary to present reports by expert professionals to provide a legal protection measure when prompted in court.
The doctor-patient relationship must include transparency, empathy and trust to reduce the patient's anxiety (97).
CONCLUSIONS
In this review, the authors sought to emphasize the actual demand for the correct diagnosis of HTSs, which differ from keloid scarring, the latter being much more difficult to treat. The evolution of more reliable and objective methods for the diagnosis and the measurement of the severity of HTSs is also essential for further inquiry in the expanse of prevention and handling. In the last few years, increased understanding of the molecular and biologic mechanisms involved in HTS germination has allowed the evolution of more than therapeutic options for these lesions. HTSs remain difficult to manage and at that place is no universally accepted treatment regimen or prove-based literature to guide their management.
Treatment begins by educating the patient well-nigh the etiology of the scarring process and must exist individualized, depending on the distribution, size, thickness and consistency of the lesions and the associated inflammation. The dr. should select the most appropriate agent according to the patient's needs and the guidelines for these signs. Nonsurgical treatment seems to be the best option most of the time. Currently, silicone gel or a silicone sheet remains the most accepted modality for the treatment and prevention of HTSs, but in many cases, there are specific indications for different types of approaches, such equally the use of pressure garments; combinations of corticosteroid injections and onion excerpt gel; bleomycin and even surgery in cases of contractures associated with the scar, mainly in burns.
Disputes concerning this topic are very far from over. Fibroproliferative disorders represent ane of the greatest puzzles in medicine and although in that location is no consensus, combination therapy has proven to be more than constructive than monotherapy. It is essential that the physician exist aware of the dissimilar therapeutic options available and be able to individualize treatment because sure patients may non respond to whatsoever single treatment modality. Finally, guidance for patients whose hypertrophic scarring usually regresses completely after half dozen months to three years would announced to be fundamental.
ACKNOWLEDGMENTS
Thanks to the Department of Pathology and Forensic Medicine of FMRP-USP for providing the histopathological photographs.
Footnotes
No potential conflict of involvement was reported.
REFERENCES
i. English RS, Shenefelt PD. Keloids and hypertrophic scars. Dermatol Surg. 1999;25(viii):631–viii. [PubMed] [Google Scholar]
2. Atiyeh BS. Nonsurgical management of hypertrophic scars: evidence-based therapies, standard practices, and emerging methods. Artful Plast Surg. 2007;31(v):468–92. [PubMed] [Google Scholar]
3. Anzarut A, Olson J, Singh P, Rowe BH, Tredget EE. The effectiveness of pressure garment therapy for the prevention of abnormal scarring after fire injury: a meta-analysis. J Plast Reconstr Aesthet Surg. 2009;62:77–84. [PubMed] [Google Scholar]
4. Leventhal D, Furr M, Reiter D. Treatment of keloids and hypertrophic scars: a meta-analysis and review of the literature. Curvation Facial Plast Surg. 2006;8(6):362–viii. [PubMed] [Google Scholar]
5. Jalali M, Bayat A. Current use of steroids in management of abnormal raised peel scars. Surgeon. 2007;v(iii):175–eighty. [PubMed] [Google Scholar]
6. Naeini FF, Najafian J, Ahmadpour One thousand. Bleomycin tattooing every bit apromising therapeutic modality in large keloids and hypertrophicscars. Dermatol Surg. 2006;32(8):1023–nine. word 1029-30. [PubMed] [Google Scholar]
vii. Leclère FM, Mordon SR. Twenty-five years of active laser prevention of scars: what take we learned. J Cosmet Light amplification by stimulated emission of radiation Ther. 2010;12:227–34. [PubMed] [Google Scholar]
8. O′Brien Fifty, Pandit A. Silicon gel sheeting for preventing and treating hypertrophic and keloid scars. Cochrane Database Syst Rev. 2013;9:CD003826. [PMC free article] [PubMed] [Google Scholar]
9. Shih R, Waltzman J, Evans GR. Plastic Surgery Educational Foundation Technology Assessment Committee Review of over-the-counter topical scar treatment products. Plast Reconstr Surg. 2007;119(iii):1091–v. [PubMed] [Google Scholar]
ten. Ehrlich HP, Desmouliere A, Diegelmann RF, Cohen IK, Compton CC, Garner WL, et al. Morphological and immunochemical differences between keloid and hypertrophic scar. Am J Pathol. 1994;145(1):105–thirteen. [PMC free article] [PubMed] [Google Scholar]
11. Gauglitz GG, Korting HC, Pavicic T, Ruzicka T, Jeschke MG. Hypertrophic Scarring and Keloids: Pathomechanisms and Electric current and Emerging Treatment Strategies. Mol Med. 2011;17(1-2):113–25. [PMC gratis article] [PubMed] [Google Scholar]
12. Al-Attar A, Mess Due south, Thomassen JM, Kauffman CL, Davison SP. Keloid pathogenesis and treatment. Plast Reconstr Surg. 2006;117:286–300. [PubMed] [Google Scholar]
13. Burd A, Huang L. Hypertrophic response and keloid diathesis: ii very different forms of scar. Plast Reconstr Surg. 2005;116(seven):150e–57e. [PubMed] [Google Scholar]
xiv. Lane JE, Waller JL, Davis LS. Relationship between age of ear piercing and keloid formation. Pediatrics. 2005;115(v):1312–4. [PubMed] [Google Scholar]
15. Lee JY, Yang CC, Chao SC, Wong TW. Histopathological differential diagnosis of keloid and hypertrophic scar. Am J Dermatopathol. 2004;26(v):379–84. [PubMed] [Google Scholar]
16. Sabater-Marco V, Perez-Valles A, Berzal-Cantalejo F, Rodriguez-Serna M, Martinez-Diaz F, Martorell-Cebollada M. Sclerosing dermatofibrosarcoma protuberans (DFSP): an unusual variant with focus on the histopathologic differential diagnosis. Int J Dermatol. 2006;45:59–62. [PubMed] [Google Scholar]
17. D′Andrea F, Vozza A, Brongo Southward, Di Girolamo F, Vozza G. Dermatofibrosarcoma protuberans: experience with 14 cases. J Eur Acad Dermatol Venereol. 2001;15(v):427–9. [PubMed] [Google Scholar]
18. Kanitakis J, Euvrard S, Sebbag L, Claudy A. Trichilemmal carcinoma of the skin mimicking a keloid in a heart transplant recipient. J Heart Lung Transplant. 2007;26(6):649–51. [PubMed] [Google Scholar]
xix. Misago N, Ogusu Y, Narisawa Y. Keloidal basal cell carcinoma after radiations therapy. Eur J Dermatol. 2004;14(3):182–five. [PubMed] [Google Scholar]
twenty. Cannick Fifty, 3, Douglas G, Crater Due south, Silvery R. Nodular scleroderma: case report and literature review. J Rheumatol. 2003;30(11):2500–02. [PubMed] [Google Scholar]
21. Santiago M1, de Castro Exercise, Jr, Costa CA, Passos ES, Paixão A. Keloidal scleroderma. Clin Rheumatol. 2004;23(1):50–1. [PubMed] [Google Scholar]
22. Gonzalez-Vela MC, Val-Bernal JF, Gonzalez-Lopez MA, Drake M, Fernández-Llaca JH. Sclerotic neurofibroma: a neurofibroma mimicking sclerotic fibroma. J Cutan Pathol. 2006;33(one):47–fifty. [PubMed] [Google Scholar]
23. Verma R, Das AL, Vaishampayan SS, Vaidya South. Keloidal granuloma faciale with extrafacial lesions. Indian J Dermatol Venereol Leprol. 2005;71(5):345–7. [PubMed] [Google Scholar]
24. Krishnan RS, Hwang LY, Tschen JA, Subrt P, Hsu S. Erythema elevatum diutinum mimicking all-encompassing keloids; quiz 386. Cutis. 2001;67(5):381–five. [PubMed] [Google Scholar]
25. Chirayil PT, Jayaraj J, Kumar P. Infantile digital fibromatosis-a case written report. Burns. 2001;27(1):89–90. [PubMed] [Google Scholar]
26. Zelger BG, Sidoroff A, Zelger B. Combined dermatofibroma: co-existence of two or more than variant patterns in a single lesion. Histopathology. 2002;36(half-dozen):529–39. [PubMed] [Google Scholar]
27. Bang RL. Penile oedema induced by continuous condom catheter use and mimicking keloid scar. Scand J Urol Nephrol. 1994;28(3):333–5. [PubMed] [Google Scholar]
28. Ibrahim RE, Sciotto CG, Weidner N. Pseudoangiomatous hyperplasia of mammary stroma. Some observations regarding its clinicopathologic spectrum. Cancer. 1989;63(6):1154–sixty. [PubMed] [Google Scholar]
29. Allan A, Andersen West, Rosenbaum M. Histologic features of lichen sclerosus et atrophicus in a surgical scar. Am J Dermatopathol. 1999;21(4):387–91. [PubMed] [Google Scholar]
30. Luz-Ramos M, Munoz-Perez MA, Pons A, Ortega M, Camacho F. Acne keloidalis nuchae and tufted pilus folliculitis. Dermatology. 1997;194(one):71–3. [PubMed] [Google Scholar]
31. Hecker MS, Weinberg JM. Cutaneous cryptococcosis mimicking keloid. Dermatology. 2001;202(1):78–nine. [PubMed] [Google Scholar]
32. Ogawa R, Akaishi S, Hyakusoku H. Differential and exclusive diagnosis of diseases that resemble keloids and hypertrophic scars. Ann Plast Surg. 2009;62(6):660–4. [PubMed] [Google Scholar]
33. Rockwell WB, Cohen IK, Ehrlich HP. Keloids and hypertrophic scars: a comprehensive review. Plast Reconstr Surg. 1989;84(5):827–37. [PubMed] [Google Scholar]
34. Aarabi S, Longaker MT, Gurtner GC. Hypertrophic scar formation following burns and trauma: new approaches to treatment. PLoS Med. 2007;4(9):e234. [PMC free article] [PubMed] [Google Scholar]
35. Bombaro KM, Engrav LH, Carrougher GJ, Wiechman SA, Faucher 50, Costa BA, et al. What is the prevalence of hypertrophic scarring following burns. Burns. 2003;29(4):299–302. [PubMed] [Google Scholar]
36. Miller MC, Nanchahal J. Advances in the modulation of cutaneous wound healing and scarring. BioDrugs. 2005;19(6):363–81. [PubMed] [Google Scholar]
37. Tredget EE. Pathophysiology and treatment of fibroproliferative disorders following thermal injury. Ann N Y Acad Sci. 1999;888:165–82. [PubMed] [Google Scholar]
38. Wang J, Ding J, Jiao H, Honardoust D, Momtazi M, Shankowsky HA, et al. Human hypertrophic scar-similar nude mouse model: characterization of the molecular and cellular biology of the scar procedure. Wound Repair Regen. 2011;19(2):274–85. [PubMed] [Google Scholar]
39. Honardoust D, Varkey G, Hori K, Ding J, Shankowsky HA, Tredget EE. Small-scale leucine-rich proteoglycans, decorin and fibromodulin, are reduced in postburn hypertrophic scar. Wound Repair Regen. 2011;19(three):368–78. [PubMed] [Google Scholar]
40. Scott PG, Dodd CM, Tredget EE, Ghahary A, Rahemtulla F. Immunohistochemical localization of the proteoglycans decorin, biglycan and versican and transforming growth cistron-beta in human post-burn hypertrophic and mature scars. Histopathology. 1995;26(five):423–31. [PubMed] [Google Scholar]
41. Shah M, Foreman DM, Ferguson MW. Neutralisation of TGF-beta 1 and TGF-beta 2 or exogenous addition of TGF-beta three to cutaneous rat wounds reduces scarring. J Cell Sci. 1995;108(Pt 3):985–1002. [PubMed] [Google Scholar]
42. Nedelec B, Shankowsky H, Scott PG, Ghahary A, Tredget EE. Myofibroblasts and apoptosis in human hypertrophic scars: the effect of interferon-alpha2b. Surgery. 2001;130(5):798–808. [PubMed] [Google Scholar]
43. Moulin V, Larochelle S, Langlois C, Thibault I, Lopez-Vallé CA, Roy M. Normal skin wound and hypertrophic scar myofibroblasts have differential responses to apoptotic inductors. J Jail cell Physiol. 2004;198(3):350–8. [PubMed] [Google Scholar]
44. Farina JA, Jr, Freitas FA, Ungarelli LF, Rodrigues JM, Rossi LA. Absence of pathological scarring in the donor site of the scalp in burns: an assay of 295 cases. Burns. 2010;36(half dozen):883–90. [PubMed] [Google Scholar]
45. Forbes-Duchart 50, Cooper J, Nedelec B, Ross L, Quanbury A. Burn therapists' opinion on the awarding and essential characteristics of a burn scar outcome measure. J Burn Care Res. 2009;30(five):792–800. [PubMed] [Google Scholar]
46. Biao Cheng, Hong-Wei Liu, Xiao-Bing Fu. Update on pruritic mechanisms of hypertrophic scars in postburn patients: the potential function of opioids and their receptors. J of Burn Care & Res. 2011;32(4):e118–25. MD, PhD,* Md,†. [PubMed] [Google Scholar]
47. Aarabi S, Bhatt KA, Shi Y, Paterno J, Chang EI, Loh SA, et al. Mechanical load initiates hypertrophic scar formation through decreased cellular apoptosis. FASEB J. 2007;21(12):3250–61. [PubMed] [Google Scholar]
48. Tziotzios C, Profyris C, Sterling J. Cutaneous scarring: pathophysiology, molecular mechanisms and scar reduction therapeutics Part 2. Strategies to reduce scar formation afterward dermatologic procedures. J Am Acad Dermatol. 2012;66(1):13–24. Jaad 2012. [PubMed] [Google Scholar]
49. Wang J, Hori K, Ding J, Huang Y, Kwan P, Ladak A, et al. Price-like receptors expressed by dermal fibroblasts contribute to hypertrophic scarring. J Cell Physiol. 2011;226(5):1265–73. [PubMed] [Google Scholar]
50. Mustoe TA, Cooter RD, Gold MH, Hobbs FD, Ramelet AA, Shakespeare PG, et al. International clinical recommendations on scar direction. Plast Reconstr Surg. 2002;110(ii):560–7. [PubMed] [Google Scholar]
51. Signorini Thousand, Clementoni MT. Clinical evaluation of a new self-drying silicone gel in the handling of scars: a preliminary report. Artful Plast Surg. 2007;31(2):183–vii. [PubMed] [Google Scholar]
52. Karagoz H, Yuksel F, Ulkur Due east, Evinc R. Comparison of efficacy of silicone gel, silicone gel sheeting, and topical onion extract including heparin and allantoin for the treatment of postburn hypertrophic scars. Burns. 2009;35(8):1097–103. [PubMed] [Google Scholar]
53. Gilman TH. Silicone canvass for treatment and prevention of hypertrophic scar: A new proposal for the mechanism of efficacy. Wound Rep Reg. 2003;11(iii):235–6. [PubMed] [Google Scholar]
54. Musgrave MA, Umraw Due north, Fish JS, Gomez M, Cartotto RC. The consequence of silicone gel sheets on perfusion of hypertrophic burn down scars. J Fire Care Rehab. 2002;23(3):208–14. [PubMed] [Google Scholar]
55. Niessen FB, Spauwen PH, Robinson PH, Fidler V, Kon Thou. The utilise of silicone occlusive sheeting (Sil-K) and silicone occlusive gel (Epiderm) in the prevention of hypertrophic scar germination. Plast Reconstr Surg. 1998;102(6):1962–72. [PubMed] [Google Scholar]
56. Hirshowitz B, Ullmann Y, Har-Shai Y, Vilenski A, Peled IJ. Silicone occlusive sheeting (SOS) in the management of hypertrophic scarring, including the possible manner of action of silicone, by static electricity. Eur J Plast Surg. 1993;16(1):5–ix. [Google Scholar]
57. Har-Shai Y, Lindenbaum Due east, Tendler M, Gamliel-Lazarovich A, Feitelberg L, Hirshowitz B. Negatively charged static electricity stimulation as a possible mechanism for enhancing the involution of hypertrophic and keloid scars. Isr Med Assoc J. 1999;1(iii):203–v. [PubMed] [Google Scholar]
58. Chan KY, Lau CL, Adeeb SM, Somasundaram Due south, Nasir-Zahari M. A randomized, placebo-controlled, double-blind, prospective clinical trial of silicone gel in prevention of hypertrophic scar development in median sternotomy wound. Plast Reconstr Surg. 2005;116(4):1013–20. [PubMed] [Google Scholar]
59. Van den Kerckhove E, Stappaerts K, Boeckx W, Van den Hof B, Monstrey S, Van der Kelen A. Silicones in the rehabilitation of burns: A review and overview. Burns. 2001;27(three):205–14. [PubMed] [Google Scholar]
60. So K, Umraw N, Scott J, Campbell K, Musgrave Grand, Cartotto R. Effects of enhanced patient didactics on compliance with silicone gel sheeting and burn scar effect: A randomized prospective study. J Burn Care Rehabil. 2003;24(6):411–vii. [PubMed] [Google Scholar]
61. Bloemen MCT, Van der Veer WM, Ulrich MW, van Zuijlen PP, Niessen FB, Middelkoop E. Prevention and curative management of hypertrophic scar germination. Burns. 2009;35(4):463–75. [PubMed] [Google Scholar]
62. Linares HA, Larson DL, Willis-Galstaun BA. Historical notes on the utilize of pressure level in the treatment of hypertrophic scars or keloids. Burns. 1993;19(1):17–21. [PubMed] [Google Scholar]
63. Esselman PC, Thombs BD, Magyar-Russell G, Fauerbach JA. Burn rehabilitation: State of the science. Am J Phys Med Rehabil. 2006;85(4):383–413. [PubMed] [Google Scholar]
64. Macintyre 50, Baird One thousand. Pressure garments for utilize in the treatment of hypertrophic scars: A review of the issues associated with their use. Burns. 2006;32(one):10–v. [PubMed] [Google Scholar]
65. Puzey One thousand. The apply of force per unit area garments on hypertrophic scars. J Tissue Viability. 2002;12(ane):11–5. [PubMed] [Google Scholar]
66. Costa AM, Peyrol S, Porto LC, Comparin JP, Foyatier JL, Desmouliere A. Mechanical forces induce scar remodeling. Written report in non–pressure- treated versus pressure-treated hypertrophic scars. Am J Pathol. 1999;155(v):1671–9. [PMC free article] [PubMed] [Google Scholar]
67. Reno F, Sabbatini K, Lombardi F, Stella Thou, Pezzuto C, Magliacani G, et al. In vitro mechanical compression induces apoptosis and regulates cytokines release in hypertrophic scars. Wound Rep Reg. 2003;11(5):331–half dozen. [PubMed] [Google Scholar]
68. Reno F, Sabbatini One thousand, Stella M, Magliacani G, Cannas 1000. Effect of in vitro mechanical pinch on Epilysin (matrix metalloproteinase-28) expression in hypertrophic scars. Wound Repair Regen. 2005;xiii(three):255–61. [PubMed] [Google Scholar]
69. Engrav LH, Heimbach DM, Rivara FP, Moore ML, Wang J, Carrougher GJ, et al. 12-Year within-wound study of the effectiveness of custom force per unit area garment therapy. Burns. 2010;36(vii):975–83. [PubMed] [Google Scholar]
70. Van den Kerckhove E, Stappaerts G, Fieuws S, Laperre J, Massage P, Flour K. The assessment of erythema and thickness on burn related scars during pressure level garment therapy every bit a preventive measure for hypertrophic scarring. Burns. 2005;31(half-dozen):696–702. [PubMed] [Google Scholar]
71. Cho JW, Cho SY, Lee SR, Lee KS. Onion extract and quercetin induce matrix metalloproteinase-1 in vitro and in vivo. Int J of Mol Med. 2010;25(3):347–52. [PubMed] [Google Scholar]
72. Ho WS, Ying SY, Chan PC, Chan HH. Apply of onion excerpt, heparin, allantoin gel in prevention of scarring in Chinese patients having laser removal of tattoos: A prospective randomized controlled trial. Dermatol Surg. 2006;32(7):891–6. [PubMed] [Google Scholar]
73. Koc E, Arca E, Surucu B, Kurumlu Z. An open up, randomized, controlled, comparative written report of the effect of intralesional triamcinolone acetonide and onion extract gel and intralesional triamcinolone acetonide alone in the treatment of hypertrophic scars and keloids. Dermatol Surg. 2008;34(eleven):1507–14. [PubMed] [Google Scholar]
74. Willital GH, Heine H. Efficacy of contractubex gel in the treatment of fresh scars afterwards thoracic surgery in children and adolescents. Int J Clin Pharm Res. 1994;14(5-six):193–202. [PubMed] [Google Scholar]
75. Chanprapaph K, Tanrattanakorn South, Wattanakrai P, Wongkitisophon P, Vachiramon Five. Effectiveness of onion extract gel on surgical scars in Asians. Dermatol Res Pract. 2012;2012:212945. [PMC free commodity] [PubMed] [Google Scholar]
76. Chen MA, Davidson TM. Scar management: Prevention and handling strategies. Curr Opinion Otolaryngol Head Neck Surg. 2005;13(iv):242–7. [PubMed] [Google Scholar]
77. Niessen FB, Spauwen P, Schalkwijk J, Kon K. On the nature of hypertrophic scars and keloids: A review. Plast Reconstr Surg. 1999;104(5):1435–58. [PubMed] [Google Scholar]
78. Manuskiatti W, Fitzpatrick RE. Treatment response of keloidal and hypertrophic sternotomy scars: Comparing amid intralesional corticosteroid, 5-fluorouracil, and 585-nm flashlamp- pumped pulsed-dye light amplification by stimulated emission of radiation treatments. Curvation Dermatol. 2002;138(ix):1149–55. [PubMed] [Google Scholar]
79. Roques C. Téot L. The use of corticoids to treat keloids: A review. Int J of Depression Extrem Wounds. 2008;7(3):137–45. [PubMed] [Google Scholar]
80. George WM. Linear lymphatic hypopigmentation afterward intralesional corticosteroid injection: Report of two cases. Cutis. 1999;64(ane):61–4. [PubMed] [Google Scholar]
81. Bodokh I, P Brun. Traitement des chéloïdes par infiltrations de bléomycine. Ann Dermatol Venereol. 1996;123(12):791–4. [PubMed] [Google Scholar]
82. Bennett JM, Reich SD. Bleomycin. Ann Intern Med. 1979;90(half dozen):945–eight. [PubMed] [Google Scholar]
83. Kingdom of spain A, Solano T, Quintanilla Eastward. Bleomycin in the treatment of keloids and hypertrophic scars past multiple needle punctures. Dermatol Surg. 2001;27(one):23–7. [PubMed] [Google Scholar]
84. Templeton SF, Solomon AR, Swerlick RA. Intradermal bleomycin injections into normal homo peel. A histopathologic and immunopathologic written report. Arch Dermatol. 1994;130(5):577–83. [PubMed] [Google Scholar]
85. James MP, Collier PM, Aherne W, Hardcastle A, Lovegrove S. Histologic, pharmacologic, and immunocytochemical effects of injection of bleomycin into viral warts. J Am Acad Dermatol. 1993;28(6):933–7. [PubMed] [Google Scholar]
86. Saray Y, Gulec AT. Handling of keloids and hypertrophic scars with dermojet injections of bleomycin: a preliminary report. Int J Dermatol. 2005;44:777–84. [PubMed] [Google Scholar]
87. Crooke ST, Bradner WT. Bleomycin, a review. J Med. 1976;7(5):333–428. [PubMed] [Google Scholar]
88. Shridharani SM, Magarakis Thousand, Manson PN, Singh NK, Basak B, Rosson GD. The emerging role of antineoplastic agents in the treatment of keloids and hypertrophic scars. Register of Plastic Surgery. 2010;64(3):355–61. [PubMed] [Google Scholar]
89. Kelly AP. Medical and surgical therapies for keloids. DermatolTher. 2004;17(2):212–8. [PubMed] [Google Scholar]
90. Zoubollis CC, Blume U, Büttner P, Orfanos CE. Outcomes of cryosurgery in keloids and hypertrophic scars: a prospective sequent trial of example series. Curvation Dermatol. 1993;129(ix):1146–51. [PubMed] [Google Scholar]
91. Freshwater MF. Botulinum toxin for scars: can it work, does it work, is it worth information technology. J Plast Reconstr Aesthet Surg. 2013;66(3):e92–iii. [PubMed] [Google Scholar]
92. Romero-Valdovinos M, Cárdenas-Mejía A, Gutiérrez-Gómez C, Flisser A, Kawa-Karasik S, Ortiz-Monasterio F. Keloid skin scars: the influence of hyperbaric oxygenation on fibroblast growth and on the expression of messenger RNA for insulin like growth factor and for transforming growth factor. In Vitro Prison cell Dev Biol Anim. 2011;47(7):421–4. [PubMed] [Google Scholar]
93. Carvalho GF, Silva RMV, Mesquita-Filho Joaquim JT, Meyer PF, Ronzio OA, Medeiros JO, et al. Avaliação dos efeitos da radiofrequência no tecido. RBM – Rev Bras Med. Edição Especial Dermatologia&Cosmiatria. 2011;68:10–25. [Google Scholar]
94. Hudson DA, Renshaw A. An algorithm for the release of burn contractures of the extremities. Burns. 2006;32(6):663–8. [PubMed] [Google Scholar]
95. Aldunate JLCB, Fontana LPMVC, Ferreira MC. Apply of dermal matrix and negative pressure dressings for the treatment of contractures in burn patients. Rev Bras Cir Plást. 2012;27(3):369–73. [Google Scholar]
96. Silva MMA, Furtado FMGP, Hochman B, Ferreira ML. Recidiva de quelóides: o estresse psicológico como fator de risco. Rev Bras Cir Plást. 2012;27(supl):one–102. [Google Scholar]
97. Jaimovich CA, Neto MK, Almeida AHT, Pinheiro AG, Loma DC. Consentimento informado east cirurgia plástica. Rev Bras Cir Plást. 2007;22(3):188–93. [Google Scholar]
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Abnormally Raised Or Thickened Scar,
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