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Photoaging and Pigmentary Changes of the Skin 3 Susan C Chapter 3 Photoaging and Pigmentary Changes of the Skin 3 Susan C. Taylor Contents Core Messages 3.1 Introduction . 29 í Several mechanisms and mediators 3.2 Mechanisms of Aging . 31 appear to control human aging, in- cluding longevity genes, cell death me- 3.3 Clinical Characteristics of Photoaging diated by telomere shorting, and free and Pigmentary Changes . 33 3.3.1 Asian Skin . 34 radical activation. 3.3.2 African American Skin . 36 3.3.3 Caucasian Skin . 38 í Clinical characteristics such as pig- mentary changes and photoaging 3.4 Histology of Photoaged Skin . 41 overshadow those of intrinsic aging. 3.4.1 The Pigmentary System Pigmentary changes are major compo- in Photoaged Skin . 43 nents of photoaging in the major skin 3.5 Overview of Prevention of Photoaging types, including Asian, African Ameri- and Pigmentary Changes of the Skin .44 can, and Caucasian. 3.6 Overview of Treatment of Photoaging and Pigmentary Changes of the Skin .45 í Intrinsic aging is marked by atrophy 3.7 Summary . 48 of the epidermis and dermis whereas References . 49 photoaging is marked by dysplasia of epidermal cells, melanocyte heteroge- neity, and elastosis of the dermis. í Features of photoaging, including pig- 3.1 Introduction mentary changes, may be prevented by limiting ultraviolet (UV) light expo- The inevitable process of aging begins at the sure. time of birth. With maturity, the features of in- trinsic or chronological aging become appar- í Use of sunscreen to block both UVA ent. The cutaneous manifestations of chrono- and UVB light is an important preven- logical aging are manifold and include a tative measure. smooth, pale appearance of the skin with fine wrinkling and loss of hydration [1]. The charac- í Antioxidants most likely play a role in teristics of intrinsic aging are often overshad- the prevention of photoaging. owed by those of photoaging. Photoaging, ag- ing of the skin induced by repeated exposures to ultraviolet (UV) light, leads to dramatic changes in the skin. These differences are high- lighted by twin studies performed by New York City plastic surgeon Dr. Darrick E. Antell in which one twin with a significant sun exposure 30 Susan C.Taylor history displayed dramatic wrinkling com- Asians, African Americans, and Caucasians. pared with her sun-protected twin (Fig. 3.1a,b). Epidermal melanin content and melanosomal Clinical characteristics of photoaging include distribution mediates the damaging effect of fine and coarse wrinkling, roughness, dryness, UV light and accounts for much of the differ- telangiectasia, cancerous lesions, precancerous ence. The mean protective factor for UVA and lesions, and pigmentary alterations. Pigmen- UVB (which is equivalent to endogenous sun 3 tary alterations are a major component of pho- protection factor) differs quite substantially toaged skin and may be observed all skin types between whites and blacks [3]. Additionally, in- [2]. Pigmentary alterations associated with dividual sun exposure habits strongly influence photoaged skin are of several varieties, includ- the degree of photodamage, with those individ- ing hypermelanosis as well as hypomelanosis. uals with greater sun exposure experiencing Mottled hyperpigmentation, ephelides, lenti- greater photodamage. Racial and ethnic vari- gines, and pigmented seborrheic keratoses are ability in photoaging is noted in relation to the the primary lesions of hypermelanosis. Guttate degree of wrinkling of the skin as well as with hypomelanosis, presenting as white spots, is the the type of pigmentary lesions that develop. primary manifestation of hypomelanosis asso- Both intrinsic aging and photoaging are ciated with aged skin. complex processes. Histological characteristics Intrinsic aging occurs universally in individ- of intrinsic aging and photoaging have been uals of all racial and ethnic groups and with all studied via electron and light microscopy. Fur- skin types. In contrast, there is variability in the thermore, an understanding of the underlying severity and manifestations of photoaging in mechanisms responsible for aging is being Figs. 3.1a,b. The manifestations of photoaging after repeated exposures to ultraviolet light are highlighted by twin studies performed by New York City plastic surgeon Dr. Darrick E. Antell in which one twin with a significant sun- exposure history displays dramatic wrinkling (a) compared with her sun-protected twin (b) Photoaging and Pigmentary Changes of the Skin Chapter 3 31 achieved. This includes genetic as well as envi- to stresses such as ultraviolet radiation, oxida- ronmental factors. Advances in both invasive tive damage, starvation, and temperature ex- and noninvasive therapeutic modalities for the tremes.There are conceivably many ways to im- treatment of photoaging have lead to the bur- pact these genetic processes and improve lon- geoning field of cosmetic dermatology. These gevity, such as caloric restriction, which may aspects will be discussed in this chapter, with potentially affect metabolic control and stress. an emphasis on the pigmentary changes of Many human homologs of the longevity genes photoaging. found in lower organisms have been identified and are currently being studied [5]. It is pro- posed that manipulation of these genes might 3.2 Mechanisms of Aging improve human longevity. The fact that genes play a crucial role in ag- In the past decade, scientific research has made ing is supported by genetic disorders in which astounding progress in elucidating the mecha- the aging process is greatly altered, such as in nism of aging of the human body, including the Werner’s syndrome. Werner’s syndrome, a dis- integument.As one might expect,aging appears order of premature aging, is characterized by to be due to a composite of genetic as well as many features, including an aged appearance, environmental factors. There appear to be sev- premature canities, alopecia, skin atrophy, cata- eral mechanisms and mediators that control racts, arteriosclerosis, and death before age 50. the multiple components of the human aging Evaluation of individuals with this syndrome process. For example, in several lower species, has provided insight into one possible genetic the genes controlling longevity have been suc- mechanism of aging. The Werner’s syndrome cessfully identified; corresponding genes are gene, which was cloned by Yu, has been identi- now being investigated in humans. Derange- fied as a DNA helicase [6]. Defective DNA me- ments in the genes that control premature ag- tabolism as a result of the Werner’s syndrome ing syndromes have been identified and pro- mutation is felt to be responsible for premature vide insight into the mechanism of aging.Chro- aging in these individuals. In progeria, another mosomal structures responsible for cell senes- genetic disorder of accelerated aging, a misreg- cence are known to play a crucial role in both ulation of mitosis has been identified as the intrinsic and photoaging. Furthermore, the role mechanism of premature aging [7].An analysis of free radicals in the aging process has been of fibroblast mRNA levels in progeria patients long recognized. Finally, the likely molecular revealed misregulation of structural, signaling, mechanism whereby UV light produces cellular and metabolic genes. Thus, several different damage leading to photoaging has been eluci- genes may be responsible for various aspects of dated. Each of these components, as outlined aging. below, will lead to a more complete under- Much attention has been given to genetically standing of the complex process of aging in hu- programmed cell death as the final common mans. pathway to aging. Cellular senescence, the in- Although a gene that controls the overall ag- ability of cells to divide indefinitely (cell death), ing process has not been identified in humans, occurs as a result of intrinsic aging as well as in organisms such as fungi,yeast,and fruit flies, photoaging. Cell senescence is controlled by 35 genes that determine life span have been telomeres. Telomeres are the repeating DNA cloned [4]. These genes are responsible for base sequences thymine-thymine-adenine- many different functions, suggesting that there guanine-guanine-guanine (TTAGGG) at the are multiple mechanisms of aging. In the lower ends of chromosomes [8]. They are thousands organisms studied, Jazwinski identified four of base pairs long and protect the ends of each principle processes responsible for aging, chromosome from damage. Shortening of the which include: metabolic control, resistance to telomere has been demonstrated in older stress, gene dysregulation, and genetic stability. adults, compared with younger individuals, and Some of the longevity genes identified respond in individuals with premature aging as in 32 Susan C.Taylor Werner’s syndrome, thus supporting the im- proteins, which leads to damage of those com- portance of telomeres in aging [9, 10]. With ponents. The damage done by free radicals con- each round of cell division, telomeres become tributes to aging. Both intrinsic and extrinsic shorter and shorter until a point is reached aging generate free radicals through either when the cell is no longer able to divide and cell internal oxidative metabolism or through ex- death occurs. There is a folded structure at the ternal environmental factors, including pollu- 3 very end of the telomere that consists of an ar- tion, cigarette smoking, and UV radiation [19]. ray of 150–200 single-stranded bases referred A common pathway involving telomeres links to as the 3′ overhang [11]. The 3′
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