Cutaneous Photoaging

Rachel E B Watson, Christopher E M Griffiths, Rachel E B Watson, Christopher E M Griffiths

• Publisher: Royal Society of Chemistry
• Year: 2019
• ISBN:
  9781788018609
• Edition: 1
• Topic: Ciencias biológicas
• Subtopic: Bioquímica

Photoaging results from chronic exposure to UV radiation and is an increasingly common clinical feature, with an aging population the clinical burden is likely to increase despite advances in our understanding of the pathology and development of improved treatments. This book will present and review the latest progress from the forefront of translational research in cutaneous photoaging. The core chapters focus on the current understanding of the biochemical mechanisms of photoageing and lead on to aspects of photoprotection and photomedicine to provide a complete picture of the current field and a context for the importance of the basic mechanistic understanding. With a global team of authors Cutaneous Photoaging provides an international perspective on the causes, consequences, pathophysiology and treatment of photoaging, ideal for dermatologists, students and professionals in photoscience.

CHAPTER 1

Photoaging in Caucasians

Jean Ayer ^a and Christopher E. M. Griffiths^*a , ^*b

^a The Dermatology Centre, Salford Royal NHS Foundation Trust, UK

^b The Centre for Dermatology Research, University of Manchester, NIHR Manchester Biomedical Research Centre, Manchester, UK,
^*E-mail: [email protected]

This chapter discusses the prevalence of photoaging in white Northern Europeans, as well as describing the two main facial photoaging phenotypes, termed ‘hypertrophic’ photoaging (HP) and ‘atrophic’ photoaging (AP). HP individuals have deep, coarse wrinkles, whereas those with AP have relatively smooth, unwrinkled skin with pronounced telangiectasia. Both phenotypes have distinct histological characteristics. AP has a significantly thicker epidermis than HP. Further stratification by gender demonstrates that the AP epidermal thickness is increased significantly in males as compared to females. HP photoaged skin exhibits severe solar elastosis, characterized by extensive deposition of amorphous, abnormally thickened, curled and fragmented elastic material in the dermis. In AP photoaged skin, there are gender differences in elastic fibre deposition; solar elastosis is apparent in females but not in males. Loss of papillary dermal fibrillin-rich microfibrils is a distinctive feature of photoaging occurring in both HP subjects and in AP females. It is important for clinicians to recognize that these two phenotypes exist because individuals with the AP phenotype have an increased propensity for developing keratinocyte cancers. Lastly, tools for measuring and objectively assessing response of photoaged skin to treatment exist and should be used for these purposes.

1.1 The Scope of the Photoaging Problem

Photoaging occurs as a result of exposure to environmental and artificial radiation and involves the superimposition of these extrinsic changes on a background of intrinsic aging. It has become significantly more prevalent in recent years due to changes in social behaviours, leisure activities, lifestyle, travelling and holiday homes abroad. ¹ Most studies outlining the incidence of photoaging have been reported from Australia, the USA and the UK. Photoaging may account for 90% of age-associated skin problems in both men and women. ^2,3 In an Australian study, clinical changes of moderate to severe photoaging were observed in 72% of men and 47% of women under 30 years of age. ⁴ The severity of photoaging directly correlates with advancing age. Even brief, intermittent sun exposure occurring while conducting activities of daily living appeared to add significantly to an average individual's daily ultraviolet radiation (UVR) exposure. ⁵ A Northwest England survey concluded that sun exposure received during normal daily activities may be sufficient to produce skin malignancies in a significant proportion of the population. ⁶

The degree of photoaging is significantly affected by an individual's ethnicity and Fitzpatrick phototype. Fair-skinned individuals of Northern European descent (Fitzpatrick phototypes I–III) are more prone to photoaging than individuals with skin of colour (Fitzpatrick phototypes IV–VI; including people of African, African-American, Asian, and Latino/Hispanic descent), ⁷ with melanin affording protection against sun-induced damage.

Among white Northern Europeans, facial photoaging comprises two distinct phenotypes, termed ‘hypertrophic’ photoaging (HP) and ‘atrophic’ photoaging (AP). ⁸ In individuals with HP, deep coarse wrinkles predominate, whereas those with AP have relatively smooth, unwrinkled skin with pronounced telangiectasia. ⁹ Both phenotypes have distinct histological characteristics. AP has a significantly thicker epidermis than HP. ⁸ Further stratification by gender demonstrates that the AP epidermal thickness is significantly increased in males as compared to females. ¹⁰ HP photoaged skin exhibits severe solar elastosis, characterized by extensive deposition of amorphous, abnormally thickened, curled and fragmented elastic material in the dermis. In AP photoaged skin, there are gender differences in elastic fibre deposition, in that solar elastosis is apparent in females but not in males. ¹⁰ Loss of papillary dermal fibrillin-rich microfibrils is a distinctive feature of photoaging and occurs in both HP subjects and in AP females but not in AP males. ¹⁰ It is important for clinicians to recognize that these two distinct phenotypes exist, because individuals with the AP photoaging phenotype have an increased propensity for developing keratinocyte cancers.

The evidence presented here is intended to demonstrate how AP and HP facial photoaging represent distinct clinical and histological entities. In HP skin, the manifestation of wrinkles, the destruction of fibrillin-rich microfibrils and the deposition of elastotic material within the dermis could act synergistically to protect against development of keratinocyte cancers. In contrast, AP males lack coarse wrinkles and solar elastosis yet retain fibrillin-rich microfibrils – all of which may act to promote keratinocyte carcinogenesis. This is an aspect of skin aging and photocarcinogenesis that warrants further exploration.

1.2 Introduction

The skin undergoes two forms of aging: (i) intrinsic or chronological aging, which occurs in its purest sense in sun-protected sites; and (ii) extrinsic aging, mainly induced by chronic exposure to ultraviolet radiation (UVR). Photoaging is the inevitable superimposition of extrinsic, i.e. photodamage on a background of intrinsic aging. ^11,12 Table 1.1 summarizes the comparison between the features of intrinsically aged and extrinsically aged skin.

Table 1.1 Features of intrinsic and extrinsic aging. Data from ref. 27

Features	Intrinsic aging	Extrinsic aging
Clinical appearance
	Smooth, unblemished	Nodular, leathery, blotchy
	Fine wrinkling	Deep wrinkling
Epidermis
Thickness	Thinner than normal	Hyperplasia in early stages, and atrophy in end stages
Proliferative rate	Lower than normal	Higher than normal
Basal keratinocytes	Modest cellular irregularity	Marked heterogeneity
Keratinization	Unchanged	Numerous dyskeratoses
Dermal–epidermal junction	Loss of rete pegs, flat, modest reduplication of lamina densa	Loss of rete pegs, flat extensive reduplication of lamina densa
Dermis
Grenz zone	Absent	Prominent
Elastin	Elastogenesis followed by elastolysis	Marked elastogenesis followed by massive degeneration – dense accumulations in dystrophic elastic fibres
Collagen	Modest change in bundle size and organization	Modest change in bundle size
Microvasculature	Normal architecture	Abnormal architecture
Inflammatory cells	No evidence of inflammation	Perivenular, histiolymphocytic infiltrate

1.3 Intrinsic Aging

Intrinsic aging is defined by the clinical, histological and physiological decrements that occur in sun-protected areas of skin of older individuals. It affects: the rate of epidermal turnover; ¹³ the thickness and cellularity of the dermis; ^14,15 re-epithelization after wound healing; immune responsiveness; ¹⁶ vitamin D synthesis; ¹⁷ and vascular reactivity. ¹⁸ There is a paucity of hair follicles, sweat glands and sebaceous glands. ^19,20 The signs of intrinsic aging begin at around 50–60 years of age, earlier in women than men, ²¹ which is attributed to menopause and a decrease in oestrogen-protective effects on the skin. ^22,23 Clinically, intrinsically aged skin appears dry and pale, smooth, thin, transparent, unblemished, and finely wrinkled due to gravitational and conformational forces. It displays a certain degree of laxity and regular pigmentation as well as an increased chance of developing a variety of epithelial neoplasms. ²⁴ Fine wrinkles associated with intrinsic aging can occur anywhere on the body surface due to loss of elasticity. Skin sagging also occurs, ^11,25,26 but the skin also maintains its youthful geometric surface patterns. ¹² The heterogeneity of pigmentation is mild in comparison to photoaging. ²⁶

1.3.1 Histological Changes o...