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CHAPTER 6 PHOTOAGING 37
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Adapted from Glogau RG Chemical peeling and aging skin J Geriatric Dermatol 1994;2(1):31
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FIGURE 6-7 Hematoxylin and eosin (H and E) stain of sun-damaged skin demonstrates sign cant elastosis in the dermis and multiple solar lentigos (Image courtsey of George Ioannides, MD)
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the other hand, respond to stressful stimuli such as UV light, osmotic shock, or cytokines,23 and are involved in cellular apoptosis24 In addition, p38 kinase is activated via stress-induced stimuli It has been demonstrated that a synchronized inhibition of ERKs and activation of JNK/p38 must be present for cellular apoptosis, suggesting that a balance among these groups influences cell survival versus death25 The MAPKs have been implicated in both intrinsic and extrinsic aging of skin Chung et al demonstrated that JNK activity is higher and ERK activity lower in intrinsically aged skin26 As previously mentioned, the combination of UV-induced c-jun
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(through the JNK pathway), and naturally expressed c-fos produces AP-1, which promotes the degrading of collagen and the extracellular matrix by increasing MMPs27 AP-1 has an additional impact in collagen loss by decreasing collagen I gene expression28 Therefore, some collagen reduction in photoaged skin may be explained by the role of AP-1 in both increasing MMPs and decreasing collagen synthesis ELASTIN Changes in elastic fibers are so characteristic in photoaged skin that elastosis, an accumulation of amorphous elastin material, is considered a hallmark of photoaged skin Thickening
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and coiling of elastic fibers in the papillary dermis distinguish the alterations induced by UV exposure Continued UV exposure leads to these same changes in the reticular dermis29 Electron microscopy examination of the elastic fibers reveals an increase in the complexity of the shape and arrangement of the fibers, a decrease in the number of microfibrils, a higher number of electron-dense inclusions, and more interfibrillar areas30 Elastin extracted from the skin of elderly patients has been shown to contain small amounts of sugar and lipids and an abnormally high level of polar amino acids3 The mechanism of these changes is not as well understood as it is in collagen; however, MMPs likely play a role because MMP-2 has been shown to degrade elastin31 It is known that the initial response of elastic fibers to photodamage is hyperplastic, resulting in increased elastic tissue The magnitude of this response depends on the degree of sun exposure The second phase of response, seen in aged elastic fibers, is degenerative, resulting in reduced elasticity and resiliency of the skin32,33 Aged skin that has suffered this degenerative response manifests an alteration in the normal pattern of immature elastic fibers, called oxytalan, which are found in the papillary dermis In young skin, these fibers form a network that ascends perpendicularly from the uppermost portion of the papillary dermis to just below the basement membrane (Fig 2-5 in 2) As skin ages, this network gradually disappears34 In fact, a loss of skin elasticity has been shown to incrementally increase with age35 This loss of elasticity may account for much of the sagging often seen in the skin of elderly individuals GLYCOSAMINOGLYCANS Glycosaminoglycans (GAGs) are important molecules because they can bind water up to 1000 times their volume The GAG family includes hyaluronic acid (HA), chondroitin sulfate, and dermatan sulfate, among many other constituents Numerous studies report that GAGs, especially HA, are decreased in amount in photoaged skin36 However, some conflicting studies report no change in the amount of GAGs in aged skin37 A study by Uitto demonstrated that photoaged skin exhibits a reduction in HA and an increase in chondroitin sulfate proteoglycans,38 which, interestingly, is a pattern also seen in scars In young skin, the HA is found at the
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