Skin Aging at a Glance
- Intrinsic (chronologic) aging occurs throughout the skin and causes primarily functional losses.
- Caused by oxidative damage, cell senescence, amino acid racemization, nonenzymatic glycosylation of proteins.
- Displays flattening of the dermal–epidermal junction, decreased cellularity, decreased dermal thickness, loss of vascular and lymphatic beds.
- Photoaging is the superposition of chronic ultraviolet-induced damage on intrinsic aging and accounts for most age-associated changes in skin appearance.
- Triggered by receptor signaling, mitochondrial damage, and protein oxidation.
- Displays variable epidermal thickness, dermal elastosis, decreased/fragmented collagen, increased matrix degrading metalloproteinases, inflammatory infiltrate, and vessel ectasia.
- Dermatologic problems with increased incidence in the elderly include skin cancer, xerosis, pruritus, varicella-zoster infection, ulcers, bullous pemphigoid, and drug eruptions.
In both developed and developing nations, the number and proportion of older people are increasing. In 2008, 23% of the US population was 55 years of age or older.1 The number of persons aged ≥65 years is expected to increase to an estimated 71 million in 2030.1,2 This demographic shift compels health care providers and government officials to confront the pathophysiology of aging and associated health issues.
Aging is a process of progressive decreases in the maximal functioning and reserve capacity of all organs in the body, including the skin. This naturally occurring functional decline in the skin is often compounded and accelerated by chronic environmental insults, such as ultraviolet (UV) and infrared (IR) irradiation as well as environmental carcinogens present in polluted air of major urban centers.
Aging occurs at the cellular level and reflects both a genetic program and cumulative environmentally imposed damage. Mammalian cells can undergo only a limited number of cell divisions and then arrest irreversibly,3–5 in a state known as replicative senescence, after which they are refractory to mitogenic stimuli. This fact has led to the perception that aging evolved in multicellular organisms as a cancer prevention mechanism6 because it prevents the unlimited and possibly unregulated growth of cells whose DNA has been progressively damaged over their life span. Of note, in general the more proficient the DNA repair mechanisms of the organism, the longer its life span.7 Furthermore, there is an inverse correlation between the organism's life span and metabolic rate,8 consistent with the understood role of cumulative oxidative DNA damage, due to aerobic metabolism, in the aging process.7
Telomeres, the terminal portions of eukaryotic chromosomes, consist of up to many hundreds of tandem short sequence repeats (TTAGGG in all mammals). During mitosis of somatic cells, DNA polymerase cannot replicate the final base pairs of each chromosome, resulting in progressive shortening with each round of cell division. A special reverse transcriptase, telomerase, can replicate these chromosomal ends, but, with the exception of stem cells and germline cells, the enzyme is normally expressed at extremely low levels. Telomeres of patients with premature aging ...