The Aging Process

Aging can be viewed as the accumulation of changes in cells and tissues resulting from a greater disorderliness of regulatory mechanisms that result in reduced robustness of the organism to encountered stress and disease. The notion of greater disorderliness in aging is illustrated by the erosion of the orderly neuroendocrine feedback regulation of the secretion of luteinizing hormone (LH), follicle stimulating hormone (FSH), adrenocorticotropic hormone (ACTH) and growth hormone (GH). These changes are manifested as menopause, andropause, adrenopause, and somatopause.

Skin aging is part of the slow decline in appearance and function that appears to be attributed in large part to the drastic decline of hormones in the body after adulthood. At the cellular level, several processes are involved in the physiology of aging and the development of some age-related diseases. The process of apoptosis signifies the process of nontraumatic and noninflammatory cell death [1].

Dysregulation of apoptosis has been implicated in the increased incidence of cutaneous malignancies that are more prevalent in older individuals, such as basal cell carcinoma, squamous cell carcinoma, and malignant melanoma. Cell senescence limits cell divisions in normal somatic cells and may play a central role in age-related diseases. Telomeres are thought to play a role in cellular aging and might contribute to the genetic background of human aging and longevity. It has been speculated that the limited proliferation potential of human cells is a result of the telomere shortening that occurs during DNA synthesis at each cell division. Photoaging may accelerate the shortening of telomeres and push cells into senescence sooner. That could be the reason why various growth factors may affect the speed and quality of wound healing [2]. Biochemical insults also arise within aging cells, in part from the action of reactive oxygen species generated and scavenged incompletely throughout the cell cycle. Aging-associated changes also occur between and among cells via alterations in the intercellular matrix, the intercellular exchange of trophic factors, the release of inflammatory cytokine mediators, and the degree of infiltration by other associated cell types. In addition, the quantity and distribution of various growth factors may affect wound healing [2].Decline of DNA repair in combination with loss of melanin increases the risk of photocarcinogenesis and can also cause the decline of enzymatically active melanocytes (10–20% each decade) that contributes to increased sensitivity to ultraviolet (UV) radiation.

However, it is not known why free radical damage does not adversely affect all of the body’s cells (e.g., gonadal germ cells) [3].