Chronic actinic damage of facial skin

Clin Dermatol. Nov-Dec 2014;32(6):752-62. doi: 10.1016/j.clindermatol.2014.02.014. Epub 2014 Feb 28.

Abstract

Chronic actinic damage of the skin manifests itself as extrinsic skin aging (photoaging) and photocarcinogenesis. During the last decade, substantial progress has been made in understanding cellular and molecular mechanisms of photoaging. DNA photodamage and ultraviolet-generated reactive oxygen species are the initial events that lead to most of the typical histologic and clinical manifestations of chronic photodamage of the skin. Chronic actinic damage affects all layers of the skin. Keratinocytes, melanocytes, fibroblasts, and endothelial cells are altered by ultraviolet radiation and can result in numerous changes in human skin, particularly the skin of fair-skinned individuals. These changes include actinic keratosis, thickening and wrinkling, elastosis, telengiectasia, solar comedones, diffuse or mottled hyperpigmentation, and skin cancers. There are many options in the treatment of changes caused by chronic actinic damage. The most effective measure of prevention of the photoaging and photocarcinogenesis is sun protection.

Publication types

  • Review

MeSH terms

  • Aging / physiology*
  • Carcinogenesis / pathology*
  • Chronic Disease
  • Facial Dermatoses / epidemiology
  • Facial Dermatoses / pathology
  • Female
  • Humans
  • Keratinocytes / metabolism
  • Keratinocytes / pathology
  • Male
  • Melanocytes / metabolism
  • Melanocytes / pathology
  • Photosensitivity Disorders / epidemiology
  • Photosensitivity Disorders / pathology*
  • Prognosis
  • Skin Aging / pathology*
  • Skin Neoplasms / epidemiology
  • Skin Neoplasms / pathology*
  • Ultraviolet Rays / adverse effects