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• W2082730061 abstract "In skin damaged severely by sunlight, a fibrillary basophilic material is present in the upper dermis1(Fig. 1). Because of staining similarities to elastin, it is referred to as solar elastosis and represents an expression of photoaging.** Photoaging is thought to be qualitatively and quantitatively different from chronological aging.2 Whereas the latter is also referred to as intrinsic aging manifested by reduced elasticity of the skin, the former is a manifestation of ‘extrinsic aging’2 resulting from damage by ultraviolet light and leading to a leathery and thickened appearing skin with deep furrows.3 Fine wrinkles occur in the background of solar elastosis4 and are the target of a vast array of cosmetic procedures employed with the aim of ‘facial rejuvenation’.5 Dermabrasion6 and laser skin resurfacing4 are among the most successful of these techniques in reducing the amount of elastotic material. As a preventive measure the long-term use of a topical ultraviolet (UV) A/B sunscreen has been shown to reduce progressive worsening of solar elastosis over time.7 What is this material composed of? Is it synthesized de novo or is it a breakdown product of normal constituents of the dermis? If it is synthesized de novo, are only fibrocytes involved or do keratinocytes and/or dermal inflammatory cells participate in the synthesis? Extensive solar elastosis (E) is noted in the upper dermis. The clinical presentations of solar elastosis are numerous and include such diverse entities as cutis rhomboidalis nuchae, Favré–Racouchot syndrome, actinic comedonal plaque, elastotic nodules of the ear, and keratoelastoidosis marginalis to name a few (reviewed in1). Histopathologically characterized by nodules, plaques or bands of elastotic material, they seem to support, at first glance, the concept that elastotic fibers are synthesized de novo and do not derive from degradation. However, as every dermatopathologist is familiar with, extensive solar elastosis as seen for example at the periphery of excision specimens of skin tumors, often goes along not only with an atrophic epidermis but also with a dermis revealing a markedly decreased thickness of its microscopically not actinically damaged portion composed of eosinophilic collagen bundles. Despite the occasional presence of large nodules of elastotic material, as seen, for example, in Favré–Racouchot syndrome and in the absence of comparative morphometric studies, it could very well be argued that elastotic nodules are derived from degradation and not from synthesis. Light, conventional and immunoelectron microscopy, immunohistochemistry, molecular biological and biochemical methods as well as the transgenic technology have been employed in order to answer questions on the composition of elastotic material and its origin. What follows is the current status of knowledge in regard to the pathogenesis of solar elastosis. One of the earliest studies on the subject was by Kligman,8 who was the first to clearly delineate age-associated changes from those induced by sunlight. He described a ‘marked hyperplasia’, thickening, curling and frequent branching of elastic fibers in sun-damaged human skin evolving into an almost complete replacement of the dermis by disorganized fibers with accompanying amorphous masses. That photoaging correlates with increased solar elastosis and is inheritably different from chronologic aging was subsequently elegantly shown in detail in a study by Bhawan et al.9 who also characterized the histopathological differences in sun-damaged skin from the face vs. the arm.10 Bouissou et al.,11 while additionally employing electron microscopy (see later), were also able to delineate the differences in photoaging and intrinsic aging. Although these light microscopical studies have greatly improved our knowledge on solar elastosis, they are however methodologically limited and can not answer the question of where the elastotic material is derived. The inverse relationship of the amount of elastotic material to collagen in actinically damaged skin as shown by Warren et al.12 can be interpreted either as an increase in the elastin synthesis and/or as an increased degradation of collagen fibers subsequently degrading to what histopathologically is perceived as solar elastosis. Electron microscopic studies performed on elastotic material in an effort to determine its essential character and source have by and large also been inconclusive. Whereas early studies by Mitchell13 and Niebauer & Stockinger14 support the hypothesis of solar elastosis being a consequence of degradation of elastin and/or collagen, the work of Berger,15 Braun-Falco16 and Marsch et al.17 seem to indicate its de novo synthesis by sun-damaged fibrocytes. More recent electron microscopical publications have been equally inconclusive.18, 19 The presence of activated fibrocytes, located close to the elastotic material and displaying a dilated rough endoplasmic reticulum and numerous secretory-like vesicles along the plasma membrane, was interpreted by Stanford et al.19 as evidence for synthesis de novo. In 1978, Nürnberger et al.20 made the same observation and came to the same conclusion. But a mere close spatial relationship of apparently metabolically very active fibrocytes to elastotic material can also be interpreted as evidence of enzyme secretion being responsible for degradation of already existing elastin and/or collagen, and thereby does not necessarily equal synthesis de novo. In a study on sun-damaged skin of five patients, Stevanovic21 noted a loss of the normal striation of collagen fibers accompanied by the surrounding deposition of a granular material. This ultrastructural observation can be interpreted as evidence of degradation and synthesis of elastotic material as well. On the contrary, Bouissou et al.11 did not find any evidence that collagen participates in the formation of elastotic material; these authors studied 104 patients. It is obvious that not only light microscopy but also conventional transmission electron microscopy is not the method of choice in providing an unequivocal answer to the question of the origin of elastotic material and its composition. The application of immunohistochemical techniques has yielded more convincing data regarding the composition of elastotic material, but determining the origin of the material requires use of biochemical and molecular biological techniques as well. In 1986, Chen et al.22 published immunohistochemical data that showed elastotic material to be composed of elastin, fibronectin, and ‘microfibrillar proteins’; immunolabeling for collagen was significantly less pronounced (in the same year, Sakai et al.23 discovered fibrillin, a 350-kDa glycoprotein and a major component of the microfibrils that surround the amorphous core of the elastic fibers. Fibrillin is a synonym for ‘microfibrillar proteins’. The amorphous core is composed of elastin). Other authors have reported immunopositivity for elastin within areas of solar elastosis but not for microfibrils themselves.18 This correlates with the inability of an antibody directed specifically against fibrillin-1 to stain those microfibrils.24 Immunopositivity within elastotic material was also found for lysozyme,24, 25 and the staining intensity seemed to correlate with the amount of sun damage.26 Glycosaminoglycans, especially hyaluronic acid and versican (a large chondroitin sulfate proteoglycan) also seem to be a component of solar elastosis as shown by immunohistochemistry and high-performance liquid chromatography.27-31 Bernstein et al.,27, 28 using confocal laser scanning microscopy, found increased glycosaminoglycans as deposits on elastotic material. In normal skin, glycosaminoglycans are situated between collagen bundles and elastic fibers; newborn skin is especially rich in dermal glycosaminoglycans, thereby giving it a myxoid appearance on conventional light microscopy. According to Bernstein et al.28 it is the abnormal location of the glycosaminoglycans that explains the weathered appearance of skin injured severely by sunlight. Based on the biochemical and immunohistochemical data now available, collagen does not seem to be a major constituent of solar elastosis.22, 32,33 Collagen gene expression is unaltered in sun-damaged skin.34 Despite the lack of immunopositivity for fibrillin-1 reported by Suwabe et al.24 and the lack of staining of elastotic material with an antimicrofibril antibody recorded by Matsuta et al.,18 Bernstein et al.3 found transcriptional up-regulation for the fibrillin gene in the cell culture of fibroblasts derived from sun-damaged skin. This finding favors the synthesis de novo of elastotic material vs. degradation of already existing connective tissue components. The use of transgenic mice in an in vivo model of photoaging is more helpful in answering the question of the origin of elastotic material.35, 36 By employing a line of transgenic mice expressing the human elastin promoter, Bernstein et al.35 observed a marked increase in promoter activity when the animals were exposed to radiation by UVB and only a moderate increase in that activity when they were exposed to UVA. The authors concluded that elastin promoter activation represents one of the primary events leading to deposits of elastotic material in human skin damaged severely by UV light. This supports the idea of de novo synthesis of solar elastosis. In cultures of dermal fibroblasts derived from the transgenic mice, irradiation by UVB led to a three-fold increase in elastin promoter activity, whereas no change was observed in their response to UVA. Bernstein et al.35 interpreted the absence of a response of dermal fibroblasts to UVA irradiation in vitro, in contrast to the induction of a response in vivo, as indicative of the role of other cells, such as mast cells, inflammatory cells, or keratinocytes in influencing the human elastin promoter response to UVA. In fact, in 1979 Lavker37 described an increased number of mast cells in human skin damaged by UV light. In mast cell-deficient mice, longstanding exposure to UVB does not lead to an increase in elastin content in the dermis, in contrast to the skin of mice not deficient in mast cells.38 The authors did not study the response to UVA. They hypothesized that mast cells are important in the development of solar elastosis, either directly by influencing the synthesis of elastin by fibroblasts or indirectly by affecting other cell types that, in turn, increase the production of elastin by fibroblasts. In vivo studies in humans, however, do not indicate a major role of mast cells in the pathogenesis of solar elastosis according to Bhawan et al.9 who were unable to detect a difference in the number of mast cells in sun-damaged vs. sun-protected skin. Elastin comprises only approximately 2–4% of the entire dermis39 and it is difficult to imagine that even a pronounced synthesis of that protein de novo could exclusively account for the abundant elastotic material that so often is seen in skin damaged severely by UV light. As Bernstein et al.3 suggested, other proteins (e.g. glycosaminoglycans, fibrillin, lysozyme) could additionally account for the deposit of elastotic material. Moreover, degradation may also play a role in the production of elastotic material. The importance of degradation in the pathogenesis of solar elastosis was shown in 1982 by Bernstein & Fonferko40 who were able to produce degeneration of elastic fibers that mimicked closely the appearance of elastotic material in sun-damaged skin. This was performed by incubation of skin from young adults with elastase and chymotrypsin. Scanning electron microscopy of elastic fibers from the skin of rats exposed to UVB light for long periods of time revealed increased tortuosity and branching of fine elastic fibers that eventually anastomosed with each other to form a tangled network.41 Furthermore, the elastolytic matrix metalloproteinases matrilysin and macrophage metalloelastase are found in solar elastosis.42 Matrilysin is derived from keratinocytes and is induced by UVB irradiation. The epidermis therefore may also play a role in the development of solar elastosis by synthesizing proteinases, which are subsequently secreted into the dermis. The absence of immunostaining for plasma proteinase inhibitors in sun-damaged skin probably indicates, according to Mera et al.,25 that the elastotic material is, at least partially, not synthesized de novo but altered. Upon review of the literature there is enough evidence to support the concept of a de novo synthesis of elastotic material as a major component in the pathogenesis of solar elastosis. The proteins synthesized include elastin, fibrillin, and glycosaminoglycans (especially hyaluronic acid and versican). However, the degradation of previously synthesized dermal matrix proteins, such as elastin and probably also collagen, seems to be involved as well. It may be that during different stages in the evolution of solar elastosis, one or the other process predominates. Not only dermal fibroblasts but also keratinocytes seem to participate in the process. However, caution has to be exercised in interpreting animal experimental data and their relevance for the pathogenesis of solar elastosis in the human, as has become clear in evaluating the role of mast cells in that process. The pathogenesis of solar elastosis is complex and not yet fully understood. Further studies are necessary." @default.
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• W2082730061 title "Pathogenesis of solar elastosis: synthesis or degradation?" @default.
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