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A combination of intravascular resin injection and formic acid incubation was utilized to study the three-dimensional arrangement of the elastic fibers in the loose connective tissue (superficial fascia) of the rat limb by scanning electron microscopy (SEM). The cast of the microvasculature served as a scaffolding for the otherwise collapsible connective tissue. SEM study demonstrated that the elastic fibers did not form an anastomosing network but were arranged in multiple layers. The fibers in each layer lay parallel to each other but were oriented differently from the fibers in the layers on either side, thereby producing a meshwork. Each individual fiber was composed of a small bundle of discrete fibrils. Some of these component fibrils separated from the parent fiber and united with other fibers, thus producing branching. The elastic fiber either decreased or grew in size by the respective sharing or joining of these component fibrils with neighboring fibers in their respective layers. Interconnections between elastic fibers of different layers were rare. These findings may provide a morphological explanation for the characteristic function of the superficial fascia, which allows the skin and underlying muscles to have a rapid and extensive alteration in their relative positions.

We studied by light and electron microscopy the elastic fibers in he sun exposed and sun protected skin of normal and psoriatic individuals of different ages in order to separate the changes of actinic damage from those of chronological aging. The sun exposed skin showed 2 types of elastic fiber abnormalities-one related to actinic damage and the other to chronological aging. The sun protected buttock skin showed only the latter. From ages 30 to 70, a minority of the elastic fibers exhibited abnormalities that appeared to represent a process of fiber disintegration. After age 70, the majority of elastic fibers showed these abnormalities. These abnormalities were present without accompanying inflammatory cells. Also, there was morphological evidence of continuing synthesis of elastic fibers during the lifetime of these subjects, except that from ages 50-93, the fibers appeared to be loosely, rather than compactly, assembled. Incubation of dermal slices from buttock skin of young adults with porcine pancreatic elastase and bovine chymotrypsin produced elastic fiber degradation that closely simulated the changes that were observed in aged sun protected skin. We propose that one of the features of cutaneous aging is a slow, spontaneous, progressive degradative process inherent in the elastic fiber that can be enzymatically accelerated from decades to hours by elastase and chymotrypsin.

In summary, the aging process in skin has at least two major manifestations: elastic fiber abnormalities involving degradation and assembly, and microvascular wall alterations of widening and atrophy depending upon the functional state of the veil cell. The abnormalities of the elastic fiber network most likely correlate with the increasing cutaneous laxity associated with aging. The microvascular abnormalities are not easily related to any specific clinical feature of aging skin. The finding of identical abnormalities in the skin of juvenile diabetics strengthens this hypothesis, as well as suggesting that these alterations are accelerated in diabetic patients. Diabetic skin might be another model system for studying cutaneous aging.

Skin signs and symptoms were examined in 46 menopausal women prior to estrogen replacement therapy. Several symptoms such as pruritus, bruising, dryness and thinning were seen more frequently in sun-exposed skin emphasizing the contribution of photoaging. At the end of a 6-mth treatment period, no significant difference was observed in the prevalence or severity of the cutaneous signs and symptoms when patients receiving transdermal 17 beta-estradiol (Estraderm) were compared with controls (the only exception was cutaneous flushing). Elastic fibers from sun-protected (buttock) skin of menopausal women were studied by light and electron microscopy. In 3 women (ages 30-37) with a history of premature menopause, the elastic fibers had several degenerative changes including coalescence of cystic spaces into lacunae, peripheral fragmentation, granular degeneration and splitting of the fibers into strands. Similar age-related ultrastructural changes are normally found in individuals that are at least 20 yrs older than these patients. These findings are suggestive of a relationship between premature aging of the dermal elastic fibers and estrogen deprivation.

In summary, the aging process in skin has at least two major manifestations: elastic fiber abnormalities involving degradation and assembly, and microvascular wall alterations of widening and atrophy depending on the functional state of the veil cell. The abnormalities of the elastic fiber network most likely correlate with the increasing cutaneous laxity associated with aging. The microvascular abnormalities are not easily related to any specific clinical feature of aging skin. The finding of identical abnormalities in the skin of juvenile diabetes strengthens this hypothesis, as well as suggesting that these alterations are accelerated in diabetic patients. Diabetic skin might be another model system for studying cutaneous aging.

To provide a morphologic basis for a better understanding of the "aging" of human skin, the authors studied the three-dimensional arrangement and chronological alterations of the fibrous components of the connective tissue using rats aged 2 weeks to 24 months with a new technique for scanning electron microscopy. These studies showed that with postnatal growth there was a dynamic rearrangement of the collagen and elastic fibers: an ordered arrangement of mature collagen bundles was attained by producing a distortion of the elastic fiber meshwork of relatively straight fibers. During adulthood, there was a subsequent tortuosity of the distorted elastic fibers coupled with an incomplete rebuilding of the elastic fiber network, laid down in a form to interlock with the collagen bundles. These changes provide a model for explaining manifestations of aged skin, such as laxity, sagging, and wrinkling. The tortuously fixed elastic fibers imply that they have been stretched and have lost their original elasticity and ability to restitute short and straight. Interlocking of both collagen and elastic fibers should disturb the two independent fibrous systems, as would normally be the case, and thus decrease tissue compliance.