Many of facial skin aging changes are not the inevitable result of chronologic aging, but with the accumulation of chronic environmental factors. The structural (molecular, cellular), histological changes and the clinical signs associated with intrinsic (chronological aging) and photoaging are discussed and summarized.

Intrinsic (Chronological) Aging

– clinically – progressively

• thinner
• drier
• less elastic
• laxity
• sag
• fine wrinkling, – genetic factors influence location and shape of facial wrinkles
• pores increase in size
• increased skin irritability
• visible coarseness
• reduced ability in epidermal cellular renewal (skin rejuvenation) and tissue repair after injury
• hair changes from vellus to terminal hair in unwanted areas.
• sebaceous gland activity decrease with aging
• increase in mechanical fragility and susceptibility to lateral shear stress
• decreased barrier function, increased susceptibility to infection

– cellular level: correlation between age and the behavior of skin cell populations – inverse relationship between age and skin cell populations – epidermal keratinocytes and dermal fibroblasts

– histological changes:

• begin with a thinning of the viable epidermis,
• flattening of the dermal-epidermal junction associated with increased amounts of water loss,
• contain basal cells with increased atypia
• probably there is enhanced diffusion through appendageal shunts or loss of integrity of the stratum corneum with aging.”
• atrophy of the dermis can be observed, significant thinning of the dermis does not appear until after 80s.
• dermis has diminished amounts of eosinophilic material
• fibroblasts appear shrunken and small
• elastic fibers can be slightly increased in thickness.

– appendages

• attenuated microvasculature: (regression and disorganization of capillaries and small vessels, with a significant reduction in the number of venular cross-sections in the skin surface) results in thinning hair
  and the pallor. Diminished blood flow impacts percutaneous absorption rates and the rate in which substances are cleared from the dermis.
• water-binding capacity and sebaceous gland activity decrease with age, the skin becomes
  drier.
• sebaceous glands hypertrophy and the changes in the adnexal structures contribute to the visible coarseness of the skin and the increased pore size, and the hair changes from vellus to terminal hair in unwanted. Sebum production falls steadily in women after menopause but remains fairly stable in men until approximately age 70 years.

Photoaging

Photo aging has its distinct clinical signs. The notion that photoaging only accelerates chronologic aging is too simplistic.

– clinical signs/morphologic changes that is not caused by chronological aging

– color:

• dyschromia and lentiges -
• progressive sallow yellow pallor
• loss of normal translucency or glow
• gradual appearance of telangiectasia and uneven purpura

– surface texture

begin with a loss of palpable smoothness, progressing to the appearance of frank keratoses, and the parallel development of fine rhytides, followed by persistent deeper folds and creases.

Clinical classification of photoaged skin by Golgau

• Type I – have no wrinkles, after 20/30, appearance of a slightly brownish cast with freckling,
• Type II wrinkles in motion – after 30/40, wrinkles begin to appear when the face is in motion. begin to have the discontinuity of the dermal elastic structure. At the same time, although lentigines are usually
  visible, epidermal atypia is manifested only by a loss of smoothness to palpation.
• Type III – have obvious wrinkles at rest, obvious visible keratoses, and sallow color that is the result of accumulated degenerated collagen and elastin,
• type IV wrinkles only: after 50s, expressive lines become permanent wrinkles. after 60/70, wrinkles begin to cover most of the facial skin.

– histological changes: the most profound differences is seen in the dermis between intrinsic and photoaging

• different from chronological aging, epidermis is generally much thicker than in either young or aged skin.
• flattening of the dermal-epidermal junction appears in both photoaged and chronologically aged skin and is considered as one of the telltale signs of aging.
• dermis has a wide band of eosinophilic material just beneath the epidermis, characterized by a mass of normal appearing
  collagen fibers. This area reveals new collagen formation indicative of decades of repair resulting from ultraviolet (UV) injury.
• fibroblasts are numerous
• hyperplastic and mast cells are abundant and degranulated indicating photoaged skin is chronically inflamed, a condition known as heliodermatitis.
• The most striking histologic feature of severely photo-damaged skin is “Elastosis” – the presence of massive quantities of thickened bundles of degraded elastic fibers. This elastotic material is
  postulated to result from UV damage to the extracellular matrix. UV damage to dermal fibroblasts produces abnormal elastin and chronic enzymatic degradation of the extracellular matrix.
• the amount of mature collagen decreases in contrast to the hypertrophy of elastin.
• the tensile strength of the looser collagen fibers increases, resulting in skin that is less stretchable.

– cellular level: epidermal keratinocytes and dermal fibroblasts with shorter lifespan in vitro culture; fibroblast senescence

– molecular level

• increased amount of type III collagen with concomitantly decreased amount of type I collagen.
• increased collagen degradation by cells of the inflammatory infiltrate found in heliodermatitis
• the ground substance composed mainly of proteoglycans is greatly increased while only moderately decreased in intrinsic aging

– appendages

• The microvasculature also is profoundly altered by chronic sun exposure. Vessel walls are thickened as a result of massive deposition of basement membrane-like
  substances. Sun-exposed vessels often are surrounded by a distinctive infiltrate of inflammatory cells. Vessels become dilated and tortuous, producing visible telangiectasias.