COSMETIC DERMATOLOGY: PRINCIPLES AND PRACTICE in .NET

Creation QR-Code in .NET COSMETIC DERMATOLOGY: PRINCIPLES AND PRACTICE

COSMETIC DERMATOLOGY: PRINCIPLES AND PRACTICE
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CHAPTER 19 Wrinkled Skin
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Sogol Saghari, MD Leslie Baumann, MD
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TABLE 19-1 Premature Aging Syndromesa SYNDROME Werner s syndrome3 Cockayne syndrome4 Progeria5 DEFECT DNA helicase DNA helicase Lamin A Decorin, a small leucine-rich proteoglycans (SLRPs) found in the extracelluar matrix protein, is involved in decorating the collagen (see 2) It is shaped in a horseshoe pattern and holds collagen fibers in the proper arrangement11 Interestingly, a fragment of decorin also known as decorunt has been shown to be higher in adult versus fetal skin12 Since decorunt has a lower affinity for collagen fibers, the breakdown of decorin to decorunt may play a role in the disorganization of the dermal collagen network seen in aged skin ELASTIN DEGRADATION Wrinkled skin is known to exhibit decreased resilience because of abnormal elastic tissue In the setting of UV exposure, the quantity of elastase, the enzyme responsible for degrading elastin, increases and leads to elastosis, a hallmark of photoaged skin However, studies have demonstrated that nonexposed aged skin also displays less elastin tissue13,14 TELOMERE SHORTENING Telomeres are the terminal portions of mammalian chromosomes that are composed of hundreds of short sequences of repeats of the base pairs TTAGGG They cap the ends of chromosomes preventing fusion15 During cell division, when the chromosomes divide, the enzyme DNA polymerase cannot replicate the final base pairs of the chromosome Therefore, these terminal sequences are continuously lost on replication, resulting in shortening of the chromosome When telomeres get too short, apoptosis of the cells is triggered For this reason, telomeres are thought to play a role in aging Telomerase is a reverse transcriptase enzyme found in stem cells that can replicate the terminal base pairs but this enzyme is not found in most cells Many studies are ongoing that are looking at the role of telomerase in aging and cancer UV exposure may contribute to telomere shortening Telomeres normally exist in a loop configuration, with the loop held in place by the final 150 to 200 bases on the 3 strand that forms a single-stranded overhang (Figs 19-1A and B) It is believed that when the loop is disrupted and the overhang becomes exposed, p53 (a tumor suppressor protein) and other DNA damage response proteins are induced,16 resulting in apoptosis or senescence UV light leads to the
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The desire to maintain or restore a youthful appearance has become a significant concern for many people in today s world Evidently, wrinkles are considered one of the major obstacles in this arena In 2004, Botox Cosmetic injections were shown to be the most often performed cosmetic procedure in the United States1 Cutaneous wrinkles, defined as furrows or ridges on the skin surface, appear to be multifactorial in etiology and a consequence of intrinsic and extrinsic aging (discussed in 6) While genetic predisposition is an important factor in developing wrinkles, engaging in particular life style behaviors such as excessive sun exposure and smoking are also known causes of cutaneous aging (see 6) This chapter will concentrate on wrinkles not caused by sun exposure but, rather, by intrinsic aging Treatment approaches focus more on the condition itself, but also address behavioral elements pertaining to extrinsic aging
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a These premature aging syndromes suggest that DNA repair capacity is very important to mitigate aging
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Pathology and Etiology
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The histopathology of wrinkles is a combination of interesting findings Epidermal thinning is an outstanding microscopic feature, where the atrophy is more prominent in the deepest area of the wrinkle (Fig 6-8) Other changes include flattening of the dermal-epidermal junction, atrophy of the subcutaneous adipose tissue of the hypodermis, as well as the loss of collagen, glycosaminoglycans, and elastin tissue COLLAGEN LOSS Abnormal and reduced collagen is a major finding in the pathology of wrinkles, both in sun-exposed and non-sun-exposed skin7 Collagen modification in wrinkled skin can be explained with a combination of different concepts It is well known that collagen synthesis is decreased in aging skin In addition, because of higher levels of matrix metalloproteinases (MMPs), collagen degradation also appears to increase with aging Another explanation for abnormal dermal collagen in cutaneous aging is collagen glycation8 As discussed in 2, glycation of collagen is a nonenzymatic process that involves the addition of a reducing sugar molecule to extracellular matrix collagen and proteins Following an oxidative reaction, the end products of glycated collagen and proteins, known as advanced glycation end products (AGEs), are formed The AGEs are then deposited on the collagen and elastin tissue, rendering them stiffer and less susceptible to contracture and remodeling In addition, glycated collagen modifies the actin cytoskeleton of fibroblasts and inhibits their contracture effect on the collagen9 AGEs can interact with certain receptors to induce intracellular signaling that leads to enhanced oxidative stress and elaboration of key proinflammatory cytokines The resulting free radicals and cytokines lead to a breakdown of collagen10
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