Causes of changes in skin texture and fine lines

Modern cosmetic medicine demands accurate recognition of all types of rhytids and their molecular causes to tailor treatment for improving aging skin appearance. This article examines the causes and treatment of fine rhytids. The underlying cause of fine lines, also known as atrophic rhytids , is dermal thinning. Myriad molecular mechanisms have been identified in the loss of dermal strength and architecture. Dermal thinning is caused by a loss of collagen and elastin in the dermis. After reviewing the histopathology of the role of dermal atrophy in the creation of fine rhytids, practitioners can better understand the prevention and treatment of fine lines. Although fine “crinkles” and lines appear superficial, the epidermis does not significantly contribute to wrinkle formation. In reality, the fine atrophic rhytids of the face are caused by molecular changes deeper in the underlying dermis. Therefore, laser rejuvenation therapies that penetrate the dermis and induce neocollagenesis and dermal remodeling are effective against the stigmata of mature skin.

As the skin ages, changes in the color, texture, and quality of the skin become apparent. Aged skin develops four different types of wrinkles: atrophic rhytids (fine lines), solar elastosis (permanent lines), dynamic expression lines, and gravitational folds. The skin becomes dry (asteatosis), yellow, rough, and leathery, with increased laxity and decreased turgor. Periorbital comedones often develop. A generalized decrease in the skin adnexal occurs, including sebaceous glands, sweat glands, and hair follicles. Changes in pigmentation may also occur, including irregular hyperpigmentation, such as sun spots or liver spots. Hypopigmentation may develop in the form of white macules called pseudoscars from excessive sun exposure. Vascular changes in the skin associated with aging include actinic purpura secondary to weak, leaky capillary beds in the dermis, and telangiectasias.

The causes of cutaneous aging can be divided into intrinsic and extrinsic causes. The intrinsic causes are simply the passage of time and genetic programming that leads to thinning of the dermis from decreased collagen and elastic dermal support systems. Normal skin aging is first noted as early as the third decade of life, with the first signs of skin fragility seen as fine shallow lines of epidermis draped over the thinning dermis. These fine lines, or atrophic rhytids, are often the first type of skin wrinkle to develop, and are a harbinger of further signs of aging skin.

Extrinsic causes of aging skin are multifactorial, and include the sequelae of environmental, behavioral, and general medical assaults on the skin. The worst offender is photoaging, also called dermatoheliosis . Signs of sun-induced skin damage may be visible as early as 15 years of age in cases of heavy childhood sun exposure. Photoaging, which certainly accelerates the normal aging process of dermal thinning and atrophic rhytid formation, is not analogous to normal aging. Photoaging also leads to a host of additional molecular and histopathologic changes in the skin architecture. For example, photoaging leads to epidermal thickening, causing a rough, dry, leathery texture. The hallmark of dermatoheliosis is elastosis, a process of haphazard hypertrophy of elastic fibers that leads to heaped-up wrinkles with deep, crisscrossing, permanent furrows. Most mature skin pigment alterations, such as hyperpigmented macules and telangiectasias, are from photoaging.