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Physiology of the Skin: Aging and Inflammation

By: Peter T. Pugliese, MD, and Michael Pugliese
Posted: February 28, 2012, from the March 2012 issue of Skin Inc. magazine.
Physiology of the Skin: Inflammation and Aging

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Histological changes of chronological aging skin show thinning of the stratum spinosum and some flattening of the dermo-epidermal junction. The sun-protected epidermis, on the other hand, shows epidermal thickness that is increased in sun-exposed skin. Why this thickness occurs remains unknown, though it is believed to be associated with some cellular mechanism that prevents apoptosis, or programmed cell death.9 Growth factors that are associated with inflammation may contribute to early tumor formation. As an example, melanocyte growths are seen as a result of the inflammatory process producing nevi and other pigmented lesions, as well as hypomelanosis, which can occur in photo-exposed areas. This accounts for a great deal of the immune damage visible after sun exposure that is intense enough to result in a burn.

In the dermal region of aging skin, a reduced number of fibroblasts are generally found, which not only produce less collagen then younger fibroblasts, but also produce more collagenase, the enzyme that destroys collagen. It appears that this is one of the major reasons that aging skin sags, as well as one of the reasons that reconstructing aging skin is so difficult. Of course, the amount of elastin in sun-damaged skin associated with aging is increased, but functionally is quite abnormal; aging skin shows histological changes that include an increased amount of cross-linking of collagen fibers.

Although this cross-linking is an enzymatic process, there is also associated nonenzymatic cross-linking that appears to be due to glycation. Both of these processes are characteristic of photodamaged skin. The amount of UV light reaching the dermis depends not only on the duration of exposure, but also on the intensity of the radiation. For example, UVA, although it penetrates deeper into the dermis than UVB, is more frequently associated with collagen damage and aging changes, while UVB damages the epidermis most frequently and is a major cause of skin cancer. The radiation intensity from UVB is 1,000 times stronger than that of UVA radiation. Skin changes resulting from chronic UV exposure show classic collagen changes with the increased levels of collagen Type III, along with abnormal, thickened, tangled and nonfunctional elastic fibers. Eventually these tissue changes result in tissue that is degenerated into a nonfibrous, amorphous mass—a finding known histologically as solar elastosis.10 It is this process that produces classic sun-damaged skin seen in inveterate sun worshipers. The bottom line is that there is no safe way to tan, because increased pigmentation appears to be a sign that some degree of inflammation has taken place.

REFERENCES

1. AA Podtelezhnikov, et al, Molecular insights into the pathogenesis of Alzheimer’s disease and its relationship to normal aging, PLoS One 6 12 :e2961 (2011)

2. SC Gupta SC, et al, Role of nuclear factor B-mediation in inflammatory pathways in cancer-related symptoms and their regulation by nutritional agents, Exp Biol Med 236 6 658–671 (Jun 1, 2011)